http://hawaiireedlab.com/labwiki/index.php?title=Special:NewPages&feed=atom&hideredirs=1&limit=50&offset=&namespace=0&username=&tagfilter=Genetics Wiki - New pages [en]2024-03-28T22:21:51ZFrom Genetics WikiMediaWiki 1.27.4http://hawaiireedlab.com/labwiki/index.php?title=L%C3%A1ruson_et_al._2018Láruson et al. 20182018-10-30T16:44:37Z<p>Floyd: </p>
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<div>=Reference=<br />
Láruson, Á. J., Coppard, S. E., Pespeni, M. H., & Reed, F. A. (2018). Gene expression across tissues, sex, and life stages in the sea urchin ''Tripneustes gratilla'' [Toxopneustidae, Odontophora, Camarodonta]. ''Marine Genomics'', 41, 12--18.<br />
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=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S1874778718300709<br />
*http://hawaiireedlab.com/pdf/l/lárusonetal2018.pdf (internal lab link only)<br />
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=Published Abstract=<br />
The pan-tropical sea urchin ''Tripneustes gratilla'' is an ecologically and economically important shallow water algal grazer. The aquaculture of ''T. gratilla'' has spurred growing interest in the population biology of the species, and by extension the generation of more molecular resources. To this purpose, de novo transcriptomes of ''T. gratilla'' were generated for two adults, a male and a female, as well as for a cohort of approximately 1000 plutei larvae. Gene expression profiles of three adult tissue samples were quantified and compared. These samples were of gonadal tissue, the neural ring, and pooled tube feet and pedicellariae. Levels of shared and different gene expression between sexes, as well as across functional categories of interest, including the immune system, toxins, genes involved in fertilization, and sensory genes are highlighted. Differences in expression of isoforms between the sexes and Sex determining Region Y-related High Mobility Group box groups is observed. Additionally an expansion of the tumor suppressor ''DMBT1'' is observed in ''T. gratilla'' when compared to the annotated genome of the sea urchin ''Strongylocentrotus purpuratus''. The draft transcriptome of ''T. gratilla'' is presented here in order to facilitate more genomic level analysis of emerging model sea urchin systems.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Hohenlohe_et_al._2012Hohenlohe et al. 20122018-10-23T09:36:14Z<p>Floyd: Created page with "=Reference= Hohenlohe, P. A., Bassham, S., Currey, M., & Cresko, W. A. (2012). Extensive linkage disequilibrium and parallel adaptive divergence across threespine stickleback..."</p>
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<div>=Reference=<br />
Hohenlohe, P. A., Bassham, S., Currey, M., & Cresko, W. A. (2012). Extensive linkage disequilibrium and parallel adaptive divergence across threespine stickleback genomes. Phil. Trans. R. Soc. B, 367(1587), 395-408.<br />
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=Links=<br />
*http://rstb.royalsocietypublishing.org/content/367/1587/395.short<br />
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=Published Abstract=<br />
Population genomic studies are beginning to provide a more comprehensive view of dynamic genome-scale processes in evolution. Patterns of genomic architecture, such as genomic islands of increased divergence, may be important for adaptive population differentiation and speciation. We used next-generation sequencing data to examine the patterns of local and long-distance linkage disequilibrium (LD) across oceanic and freshwater populations of threespine stickleback, a useful model for studies of evolution and speciation. We looked for associations between LD and signatures of divergent selection, and assessed the role of recombination rate variation in generating LD patterns. As predicted under the traditional biogeographic model of unidirectional gene flow from ancestral oceanic to derived freshwater stickleback populations, we found extensive local and long-distance LD in fresh water. Surprisingly, oceanic populations showed similar patterns of elevated LD, notably between large genomic regions previously implicated in adaptation to fresh water. These results support an alternative biogeographic model for the stickleback radiation, one of a metapopulation with appreciable bi-directional gene flow combined with strong divergent selection between oceanic and freshwater populations. As predicted by theory, these processes can maintain LD within and among genomic islands of divergence. These findings suggest that the genomic architecture in oceanic stickleback populations may provide a mechanism for the rapid re-assembly and evolution of multi-locus genotypes in newly colonized freshwater habitats, and may help explain genetic mapping of parallel phenotypic variation to similar loci across independent freshwater populations.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Silver_1993Silver 19932018-10-23T09:28:10Z<p>Floyd: </p>
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<div>=Reference=<br />
Silver, L. M. (1993). The peculiar journey of a selfish chromosome: mouse t haplotypes and meiotic drive. Trends in Genetics, 9(7), 250-254.<br />
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=Links=<br />
*https://www.sciencedirect.com/science/article/pii/0168952593900905<br />
*http://hawaiireedlab.com/pdf/s/silver1993.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Mouse t haplotypes are descendents of a variant form of chromosome 17 that evolved the ability to propagate itself at the expense of the wild-type homolog from heterozygous +/t males. Although once enigmatic, these widespread selfish chromosomes have revealed many of their secrets in response to a combined assault with molecular, genetic and phylogenetic techniques. This review summarizes the current understanding of t haplotypes and their raison d'être.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Turner_et_al._2005Turner et al. 20052018-10-23T09:21:26Z<p>Floyd: Created page with "=Reference= Turner, T. L., Hahn, M. W., & Nuzhdin, S. V. (2005). Genomic islands of speciation in Anopheles gambiae. PLoS biology, 3(9), e285. =Links= *https://journals.plos...."</p>
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<div>=Reference=<br />
Turner, T. L., Hahn, M. W., & Nuzhdin, S. V. (2005). Genomic islands of speciation in Anopheles gambiae. PLoS biology, 3(9), e285.<br />
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=Links=<br />
*https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0030285<br />
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=Published Abstract=<br />
The African malaria mosquito, ''Anopheles gambiae'' sensu stricto (''A. gambiae''), provides a unique opportunity to study the evolution of reproductive isolation because it is divided into two sympatric, partially isolated subtaxa known as ''M'' form and ''S'' form. With the annotated genome of this species now available, high-throughput techniques can be applied to locate and characterize the genomic regions contributing to reproductive isolation. In order to quantify patterns of differentiation within ''A. gambiae'', we hybridized population samples of genomic DNA from each form to Affymetrix GeneChip microarrays. We found that three regions, together encompassing less than 2.8 Mb, are the only locations where the ''M'' and ''S'' forms are significantly differentiated. Two of these regions are adjacent to centromeres, on Chromosomes 2L and X, and contain 50 and 12 predicted genes, respectively. Sequenced loci in these regions contain fixed differences between forms and no shared polymorphisms, while no fixed differences were found at nearby control loci. The third region, on Chromosome 2R, contains only five predicted genes; fixed differences in this region were also verified by direct sequencing. These “speciation islands” remain differentiated despite considerable gene flow, and are therefore expected to contain the genes responsible for reproductive isolation. Much effort has recently been applied to locating the genes and genetic changes responsible for reproductive isolation between species. Though much can be inferred about speciation by studying taxa that have diverged for millions of years, studying differentiation between taxa that are in the early stages of isolation will lead to a clearer view of the number and size of regions involved in the genetics of speciation. Despite appreciable levels of gene flow between the M and S forms of ''A. gambiae'', we were able to isolate three small regions of differentiation where genes responsible for ecological and behavioral isolation are likely to be located. We expect reproductive isolation to be due to changes at a small number of loci, as these regions together contain only 67 predicted genes. Concentrating future mapping experiments on these regions should reveal the genes responsible for reproductive isolation between forms.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Wulff_2006Wulff 20062018-10-21T09:37:31Z<p>Floyd: Created page with "=Reference= Wulff, J. L. (2006). Ecological interactions of marine sponges. Canadian Journal of Zoology, 84(2), 146-166. =Links= *http://www.nrcresearchpress.com/doi/abs/10.1..."</p>
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<div>=Reference=<br />
Wulff, J. L. (2006). Ecological interactions of marine sponges. Canadian Journal of Zoology, 84(2), 146-166.<br />
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=Links=<br />
*http://www.nrcresearchpress.com/doi/abs/10.1139/z06-019<br />
*http://hawaiireedlab.com/pdf/w/wulff2006.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Sponges interact with most other organisms in marine systems as competitors, symbionts, hosts of symbionts, consumers, and prey. Considerable creative energy has been required to study and describe the amazing variety of sponge interactions, as sponges can hide symbionts deep inside, rapidly regenerate wounds from grazers, carry on important associations with unculturable microscopic organisms, and otherwise foil attempts to determine how they are interacting with other organisms. This review of sponge interactions covers (i) competition among sponge species, and between sponges and other sessile organisms; (ii) predation on sponges by sponge specialists and by opportunistic sponge feeders, and aspects of predation such as the importance of nutritional quality, trade-offs between growth and defense against predators, biogeographic patterns in predation, and the advantages of various techniques for studying predation; and (iii) symbiotic associations of sponges with a variety of organisms representing all types of life, and with results ranging from parasitism and disease to mutual benefit. A hint that some generalizations about ecological interactions of sponges may be possible is just becoming evident, as accumulating data appear to show taxonomic and geographic patterns; however, it is also clear that surprises will continue to emerge from every probing new study.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Gonz%C3%A1lez-Rivero_et_al._2011González-Rivero et al. 20112018-10-21T08:40:18Z<p>Floyd: Created page with "=Reference= González-Rivero, M., Yakob, L., & Mumby, P. J. (2011). The role of sponge competition on coral reef alternative steady states. Ecological Modelling, 222(11), 1847..."</p>
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<div>=Reference=<br />
González-Rivero, M., Yakob, L., & Mumby, P. J. (2011). The role of sponge competition on coral reef alternative steady states. Ecological Modelling, 222(11), 1847-1853.<br />
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=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0304380011001438<br />
*http://hawaiireedlab.com/pdf/g/gonzález-riveroetal2011.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Sponges constitute an abundant and functionally important component of coral reef systems. Given their demonstrated resistance to environmental stress, it might be expected that the role of sponges in reef systems under modern regimes of frequent and severe disturbance may become even more substantial. Disturbances have recently reshaped the community structure of many Caribbean coral reefs shifting them towards a state of persistent low coral cover and often a dominance of macroalgae. Using competition and growth rates recorded from Glover's Atoll in Belize, we parameterise a mathematical model used to simulate the three-way competition between sponges, macroalgae and coral. We use the model to determine the range of parameters in which each of the three species might be expected to dominate. Emergent properties arise from our simple model of this complex system, and these include a special case in which heightened competitive ability of macroalgae versus coral may counter-intuitively prove to be advantageous to the persistence of corals. Importantly, we show that even under scenarios whereby sponges fail to invade the system, inclusion of this third antagonist can qualitatively affect the likelihood of alternative stable states – generally in favour of macroalgal dominance. The interplay between multi-species competition and predation is complex, but our efforts highlight a key process that has, until now, remained unexplored: the extent to which sponges dissipate algal grazing pressure by providing generalist fish with an alternative food source. We highlight the necessity of identifying the extent by which this process takes place in tropical systems in order to improve projections of alternative stable states for Caribbean coral reefs.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Bell_et_al._2013Bell et al. 20132018-10-21T08:28:02Z<p>Floyd: Created page with "=Citation= Bell, J. J., Davy, S. K., Jones, T., Taylor, M. W., & Webster, N. S. (2013). Could some coral reefs become sponge reefs as our climate changes?. Global Change Biolo..."</p>
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<div>=Citation=<br />
Bell, J. J., Davy, S. K., Jones, T., Taylor, M. W., & Webster, N. S. (2013). Could some coral reefs become sponge reefs as our climate changes?. Global Change Biology, 19(9), 2613-2624.<br />
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=Links=<br />
*https://onlinelibrary.wiley.com/doi/abs/10.1111/gcb.12212<br />
*http://hawaiireedlab.com/pdf/b/belletal2013.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Coral reefs across the world have been seriously degraded and have a bleak future in response to predicted global warming and ocean acidification (OA). However, this is not the first time that biocalcifying organisms, including corals, have faced the threat of extinction. The end‐Triassic mass extinction (200 million years ago) was the most severe biotic crisis experienced by modern marine invertebrates, which selected against biocalcifiers; this was followed by the proliferation of another invertebrate group, sponges. The duration of this sponge‐dominated period far surpasses that of alternative stable‐ecosystem or phase‐shift states reported on modern day coral reefs and, as such, a shift to sponge‐dominated reefs warrants serious consideration as one future trajectory of coral reefs. We hypothesise that some coral reefs of today may become sponge reefs in the future, as sponges and corals respond differently to changing ocean chemistry and environmental conditions. To support this hypothesis, we discuss: (i) the presence of sponge reefs in the geological record; (ii) reported shifts from coral‐ to sponge‐dominated systems; and (iii) direct and indirect responses of the sponge holobiont and its constituent parts (host and symbionts) to changes in temperature and pH. Based on this evidence, we propose that sponges may be one group to benefit from projected climate change and ocean acidification scenarios, and that increased sponge abundance represents a possible future trajectory for some coral reefs, which would have important implications for overall reef functioning.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Keyse_et_al._2014Keyse et al. 20142018-10-21T08:23:17Z<p>Floyd: Created page with "=Citation= Keyse, J., Crandall, E. D., Toonen, R. J., Meyer, C. P., Treml, E. A., & Riginos, C. (2014). The scope of published population genetic data for Indo-Pacific marine..."</p>
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<div>=Citation=<br />
Keyse, J., Crandall, E. D., Toonen, R. J., Meyer, C. P., Treml, E. A., & Riginos, C. (2014). The scope of published population genetic data for Indo-Pacific marine fauna and future research opportunities in the region. Bulletin of Marine Science, 90(1), 47-78.<br />
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=Links=<br />
*https://www.ingentaconnect.com/content/umrsmas/bullmar/2014/00000090/00000001/art00003<br />
*http://hawaiireedlab.com/pdf/k/keyseetal2014.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Marine biodiversity reaches its pinnacle in the tropical Indo-Pacific region, with high levels of both species richness and endemism, especially in coral reef habitats. While this pattern of biodiversity has been known to biogeographers for centuries, causal mechanisms remain enigmatic. Over the past 20 yrs, genetic markers have been employed by many researchers as a tool to elucidate patterns of biodiversity above and below the species level, as well as to make inferences about the underlying processes of diversification, demographic history, and dispersal. In a quantitative, comparative framework, these data can be synthesized to address questions about this bewildering diversity by treating species as “replicates.” However, the sheer size of the Indo-Pacific region means that the geographic and genetic scope of many species' data sets are not complementary. Here, we describe data sets from 116 Indo-Pacific species (108 studies). With a mind to future synthetic investigations, we consider the strengths and omissions of currently published population genetic data for marine fauna of the Indo-Pacific region, as well as the geographic and taxonomic scope of the data, and suggest some ways forward for data collection and collation. <br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=San_Jose_et_al._2018San Jose et al. 20182018-10-20T23:40:22Z<p>Floyd: Created page with "=Citation= San Jose, M., Doorenweerd, C., Leblanc, L., Barr, N., Geib, S., & Rubinoff, D. (2018). Incongruence between molecules and morphology: A seven-gene phylogeny of Daci..."</p>
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<div>=Citation=<br />
San Jose, M., Doorenweerd, C., Leblanc, L., Barr, N., Geib, S., & Rubinoff, D. (2018). Incongruence between molecules and morphology: A seven-gene phylogeny of Dacini fruit flies paves the way for reclassification (Diptera: Tephritidae). Molecular phylogenetics and evolution, 121, 139-149.<br />
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=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S1055790317307145<br />
*http://hawaiireedlab.com/pdf/s/sanjoseetal2018.pdf (internal lab link only)<br />
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=Published Abstract=<br />
Molecular and morphological research often suggest conflicting results. Selective pressure on certain morphologies can confound understanding of evolutionary relationships. Dacini is one of the most diverse tribes of tephritid flies and contains many economically important pest species. Their black and yellow patterned body markings are presumed to act as wasp mimicry, and the characters separating species and groups are limited and in some cases phenotypically plastic. The traditional taxonomy of the tribe is controversial because groupings are based on unique combinations of morphological characters without the use of cladistic methods, though recent phylogenetic and taxonomic analyses have resulted in significant changes to their taxonomy. The monophyly of the three largest genera in the tribe has been tested with only small numbers of representatives per genus and a limited number of genes. To further understand the taxonomy and evolution of Dacini we sequenced seven genes from 167 Dacini species and five dipteran outgroups to construct a robust phylogeny and test phylogenetic relationships between genera, subgenera, and species complexes. Our phylogeny confirms the monophyly of Dacus, Bactrocera, and Zeugodacus. However, most groups below the genus level are not monophyletic, and only through further revision will we be able to understand their evolution and clarify the taxonomy within this tribe.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Begun_and_Aquadro_1992Begun and Aquadro 19922018-10-20T23:18:13Z<p>Floyd: /* Notes */</p>
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<div>=Reference=<br />
Begun, D. J., & Aquadro, C. F. (1992). Levels of naturally occurring DNA polymorphism correlate with recombination rates in D. melanogaster. Nature, 356(6369), 519.<br />
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=Links=<br />
*https://www.nature.com/articles/356519a0<br />
*http://hawaiireedlab.com/pdf/b/begunandaquadro1992.pdf (internal lab link only)<br />
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=Published Abstract=<br />
TWO genomic regions with unusally low recombination rates in Drosophila melanogaster have normal levels of divergence but greatly reduced nucleotide diversity1,2, apparently resulting from the fixation of advantageous mutations and the associated hitchhiking effect3,4. Here we show that for 20 gene regions from across the genome, the amount of nucleotide diversity in natural populations of D. melanogaster is positively correlated with the regional rate of recombination. This cannot be explained by variation in mutation rates and/or functional constraint, because we observe no correlation between recombination rates and DNA sequence divergence between D. melanogaster and its sibling species, D. simulans. We suggest that the correlation may result from genetic hitch-hiking associated with the fixation of advantageous mutants. Hitch-hiking thus seems to occur over a large fraction of the Drosophila genome and may constitute a major constraint on levels of genetic variation in nature.<br />
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=Notes=<br />
The essential result is summarized in these two figures. <br />
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[[File:BegunAndAquadro1992Figures.png]]<br />
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Under the neutral theory diversity within a species is expected to be 4''Nμ'' (''N'' is the population size) and differences between species is expected to be 2''tμ'' (''t'' is the time of divergence in generations). Both of these are proportional to the mutation rate ''μ''. Under a simple model 4''N'' and 2''t'' are not expected to change among loci. However, the mutation rate, ''μ'', can easily change among different genes but the effect on both diversity and difference is expected to be proportional. The authors found that diversity within a species increases with rates of recombination along a chromosome, but differences between species do not. This is not consistent with the neutral theory and indicates some form of selection is acting in a general way with genome level effects. (This stands in sharp contrast to the original formulation of the neutral theory.) <br />
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The leading hypothesis is that diversity reducing selection is acting within species---and this affects a larger ragion around targets of selection in areas of lower recombination. The big question is what kind of selection. Both [[Hitchhiking]] from [[Selective Sweeps]] and [[Background Selection]] can contribute to this pattern and are not mutually exclusive. (This is related to the idea of [[Hill–Robertson Interference]].) Also, keep in mind that selective sweeps need not necessarily be adaptive. Often hitchhiking is framed in terms of adaptive evolution. However, "selfish" alleles can cause a hitchhiking effect without increasing an organism's fitness in a Darwinian sense.<br />
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There are additional hypotheses that can enhance the observed effect but these, in general, depend on an interaction with other forms of selection such as hitchhiking and background selection. One is that evolution favors locating genes that are more adaptive with higher levels of diversity, such as balancing selection at genes such as MHC and the ABO blood group, in regions of higher recombination, to promote maintaining diversity in the face of widespread diversity reducing selection. Another is that recombination is mutagenic (a higher mutation rate in regions of higher recombination)---there is evidence for this in some species---and selection is acting more efficiently in regions of higher recombination to remove slightly deleterious alleles before they can fix along the lineage leading to a species (there is theoretical support for this, but again it depends on an interaction with other forms of selection such as hitchhiking and background selection). These can be combined. For example, genes that undergo rapid evolution (such as those involved in immune response) might be more adaptive in regions of higher recombination because of the mutagenic effect of recombination---this can be independent of background selection and hitchhiking (but is not necessarily so)---, but this is unlikely to be generally true for many genes in the genome (most mutations, if they have a fitness effect, result in lower fitness; it is easier to break something than improve it when making random changes). <br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Species_DefinitionSpecies Definition2018-10-18T23:14:07Z<p>Floyd: Created page with "=Abiotic Species Concept= This is only my own view and is not shared by many biologists. Species do not exist in biological reality; it is only a label/tool used by people to..."</p>
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<div>=Abiotic Species Concept=<br />
This is only my own view and is not shared by many biologists. Species do not exist in biological reality; it is only a label/tool used by people to talk about living organisms. There is a strong correlation between many biological principles, morphological differences, boundaries to gene flow, shared ancestry, etc. between what are commonly viewed as species by humans and collections of biological organisms. This has led to attempts to unite the two and define species in biological terms, but ultimately this approach fails to be universal. This is not to say that the concept of a species does not have value. It is a tool that helps us in management and conservation decisions. However, we should accept that the relationship between human defined species and collections of biological organisms is imperfect.<br />
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...to be continued. I will also add some other types of species concepts here.</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Life_DefinitionLife Definition2018-10-18T23:08:07Z<p>Floyd: </p>
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<div>These are only my own views but I think to be living something must be able to reproduce and evolve in a heritable way. I have also tried to include a stipulation that the evolution must be open ended but this starts to get hard to define. As I see it viruses are examples of life, which put me into disagreement with many biologists. There are many other attempts to define life which I will try to collect here as well. ...to be continued...</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=BiologyBiology2018-10-18T23:05:52Z<p>Floyd: /* Definitions */</p>
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<div>=Definitions=<br />
Strangely enough biologists do not have generally accepted definitions of life or of species. I've been thinking a lot about this over the last year or so. This is a way to make notes and develop these ideas a bit. <br />
*[[Life Definition]]<br />
*[[Species Definition]]<br />
Also, I've been thinking about the human concept of what is and is not natural. I'll put some of these notes here as well. <br />
*[[Natural Definition]]<br />
Related to this is the definition of a phenotype as it relates to dominance. I've been thinking about this over the last decade. <br />
*[[Phenotype Definition]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Przeworski_et_al._2000Przeworski et al. 20002018-10-17T16:42:56Z<p>Floyd: Created page with "=Citation= Przeworski, M., Hudson, R. R., & Di Rienzo, A. (2000). Adjusting the focus on human variation. Trends in Genetics, 16(7), 296-302. =Links= *https://www.sciencedire..."</p>
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<div>=Citation=<br />
Przeworski, M., Hudson, R. R., & Di Rienzo, A. (2000). Adjusting the focus on human variation. Trends in Genetics, 16(7), 296-302.<br />
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=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0168952500020308<br />
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=Published Abstract=<br />
Studies of nuclear sequence variation are accumulating, such that we can expect a good description of the structure of human variation across populations and genomic regions in the near future. This description will help to elucidate the evolutionary forces that shape patterns of variability. Such an understanding will be of general biological interest, but could also facilitate the design and interpretation of disease-mapping studies. Here, we integrate the results from surveys of nuclear sequence variation. When nuclear sequences are considered together with mtDNA and microsatellites, it becomes clear that neither the standard neutral model, nor a simple long-term exponential growth model, can account for all the available human variation data. A possible explanation is that a subset of loci are not evolving neutrally; even so, more-complex models of effective population size and structure might be necessary to explain the data.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Marygold_et_al._2007Marygold et al. 20072018-10-17T14:32:33Z<p>Floyd: /* Links */</p>
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<div>=Citation=<br />
Marygold, S. J., Roote, J., Reuter, G., Lambertsson, A., Ashburner, M., Millburn, G. H., ... & Leevers, S. J. (2007). The ribosomal protein genes and Minute loci of Drosophila melanogaster. Genome biology, 8(10), R216.<br />
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=Links=<br />
*https://genomebiology.biomedcentral.com/articles/10.1186/gb-2007-8-10-r216<br />
*http://hawaiireedlab.com/pdf/m/marygoldetal2007.pdf (internal lab link only)<br />
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=Published Abstract=<br />
==Background==<br />
Mutations in genes encoding ribosomal proteins (RPs) have been shown to cause an array of cellular and developmental defects in a variety of organisms. In Drosophila melanogaster, disruption of RP genes can result in the 'Minute' syndrome of dominant, haploinsufficient phenotypes, which include prolonged development, short and thin bristles, and poor fertility and viability. While more than 50 Minute loci have been defined genetically, only 15 have so far been characterized molecularly and shown to correspond to RP genes.<br />
==Results==<br />
We combined bioinformatic and genetic approaches to conduct a systematic analysis of the relationship between RP genes and Minute loci. First, we identified 88 genes encoding 79 different cytoplasmic RPs (CRPs) and 75 genes encoding distinct mitochondrial RPs (MRPs). Interestingly, nine CRP genes are present as duplicates and, while all appear to be functional, one member of each gene pair has relatively limited expression. Next, we defined 65 discrete Minute loci by genetic criteria. Of these, 64 correspond to, or very likely correspond to, CRP genes; the single non-CRP-encoding Minute gene encodes a translation initiation factor subunit. Significantly, MRP genes and more than 20 CRP genes do not correspond to Minute loci.<br />
==Conclusion==<br />
This work answers a longstanding question about the molecular nature of Minute loci and suggests that Minute phenotypes arise from suboptimal protein synthesis resulting from reduced levels of cytoribosomes. Furthermore, by identifying the majority of haplolethal and haplosterile loci at the molecular level, our data will directly benefit efforts to attain complete deletion coverage of the D. melanogaster genome.<br />
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[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Benjamini_and_Hochberg_1995Benjamini and Hochberg 19952018-10-17T06:43:57Z<p>Floyd: Created page with "=Citation= Benjamini, Y., & Hochberg, Y. (1995). Controlling the false discovery rate: a practical and powerful approach to multiple testing. Journal of the Royal Statistical..."</p>
<hr />
<div>=Citation=<br />
Benjamini, Y., & Hochberg, Y. (1995). Controlling the false discovery rate: a practical and powerful approach to multiple testing. Journal of the Royal Statistical Society. Series B (Methodological), 289-300.<br />
<br />
=Links=<br />
*https://www.jstor.org/stable/2346101<br />
*http://hawaiireedlab.com/pdf/b/benjaminiandhochberg1995.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Hahn_2008Hahn 20082018-10-17T06:25:10Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Hahn, M. W. (2008). Toward a selection theory of molecular evolution. Evolution: International Journal of Organic Evolution, 62(2), 255-265.<br />
<br />
=Links=<br />
*https://onlinelibrary.wiley.com/doi/full/10.1111/j.1558-5646.2007.00308.x<br />
*http://hawaiireedlab.com/pdf/h/hahn2008.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Aedes_albopictusAedes albopictus2018-10-17T01:42:36Z<p>Floyd: </p>
<hr />
<div>*Lafferty, K. D., McLaughlin, J. P., Gruner, D. S., Bogar, T. A., Bui, A., Childress, J. N., ... & Miller-ter Kuile, A. (2018). Local extinction of the Asian tiger mosquito (Aedes albopictus) following rat eradication on Palmyra Atoll. Biology letters, 14(2), 20170743.<br />
<br />
[[Category:Organism]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=S%C3%A9ralini_et_al._2014Séralini et al. 20142018-10-16T15:29:14Z<p>Floyd: </p>
<hr />
<div>=Citation=<br />
Séralini, G. E., Clair, E., Mesnage, R., Gress, S., Defarge, N., Malatesta, M., ... & de Vendômois, J. S. (2014). Republished study: long-term toxicity of a Roundup herbicide and a Roundup-tolerantgenetically modified maize. Environmental Sciences Europe, 26(1), 14.<br />
<br />
=Links=<br />
*https://enveurope.springeropen.com/articles/10.1186/s12302-014-0014-5<br />
*http://hawaiireedlab.com/pdf/s/séralinietal2014.pdf (internal lab link only)<br />
<br />
=Notes=<br />
Republished from [[Séralini_et_al._2012]]. <br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=S%C3%A9ralini_et_al._2012Séralini et al. 20122018-10-13T01:23:20Z<p>Floyd: /* Notes */</p>
<hr />
<div>=Citation=<br />
Séralini, G. E., Clair, E., Mesnage, R., Gress, S., Defarge, N., Malatesta, M., ... & De Vendômois, J. S. (2012). RETRACTED: Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize.<br />
<br />
=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0278691512005637<br />
*https://www.ncbi.nlm.nih.gov/pubmed/27752412<br />
*https://en.wikipedia.org/wiki/S%C3%A9ralini_affair<br />
*http://hawaiireedlab.com/pdf/s/séralinietal2012.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
==BACKGROUND==<br />
The health effects of a Roundup-tolerant NK603 genetically modified (GM) maize (from 11% in the diet), cultivated with or without Roundup application and Roundup alone (from 0.1 ppb of the full pesticide containing glyphosate and adjuvants) in drinking water, were evaluated for 2 years in rats. This study constitutes a follow-up investigation of a 90-day feeding study conducted by Monsanto in order to obtain commercial release of this GMO, employing the same rat strain and analyzing biochemical parameters on the same number of animals per group as our investigation. Our research represents the first chronic study on these substances, in which all observations including tumors are reported chronologically. Thus, it was not designed as a carcinogenicity study. We report the major findings with 34 organs observed and 56 parameters analyzed at 11 time points for most organs.<br />
==RESULTS==<br />
Biochemical analyses confirmed very significant chronic kidney deficiencies, for all treatments and both sexes; 76% of the altered parameters were kidney-related. In treated males, liver congestions and necrosis were 2.5 to 5.5 times higher. Marked and severe nephropathies were also generally 1.3 to 2.3 times greater. In females, all treatment groups showed a two- to threefold increase in mortality, and deaths were earlier. This difference was also evident in three male groups fed with GM maize. All results were hormone- and sex-dependent, and the pathological profiles were comparable. Females developed large mammary tumors more frequently and before controls; the pituitary was the second most disabled organ; the sex hormonal balance was modified by consumption of GM maize and Roundup treatments. Males presented up to four times more large palpable tumors starting 600 days earlier than in the control group, in which only one tumor was noted. These results may be explained by not only the non-linear endocrine-disrupting effects of Roundup but also by the overexpression of the EPSPS transgene or other mutational effects in the GM maize and their metabolic consequences.<br />
==CONCLUSION==<br />
Our findings imply that long-term (2 year) feeding trials need to be conducted to thoroughly evaluate the safety of GM foods and pesticides in their full commercial formulations.<br />
<br />
=Notes=<br />
Republished as [[Séralini et al. 2014]]. <br />
<br />
I plan to write a more detailed discussion of these results, but do not have time at the moment. Long story short I do not think the results back up the claims made. I use this paper as a teaching tool in my undergraduate genetics class (how to read these graphs and evaluate the results, with more background information than what is here at the moment). <br />
<br />
[[File:Séralinietal2014figure4.jpg]] <br />
<br />
Published caption: "Figure 4 Largest non-regressive tumors in rats fed GMO treated or not by Roundup andeffects of Roundup alone. Rats were fed with NK603 GM maize (with orwithout application of Roundup) at three different doses (11%, 22%, and 33% intheir diet; thin, medium, and bold lines, respectively) compared to thesubstantially equivalent closest isogenic non-GM maize (control, dotted line).Roundup was administered in drinking water at three increasing doses, samesymbols, environmental (A), MRL in some agricultural GMOs (B),and half of minimal agricultural levels (C), see ‘Methods’).The largest tumors were palpable during the experiment and numbered from 20 mmin diameter for males and 17.5 mm for females. Above this size, 95% of growthswere non-regressive tumors. Summary of all tumors are shown in the barhistograms: black, non-regressive large tumors; white, small internal tumors;grey, metastases."<br />
<br />
[[File:Séralinietal2014figure6.jpg]]<br />
<br />
Published caption: "Figure 6 Mortality of rats fed GMO treated or not with Roundup and effects of Roundupalone. The symbols of curves and treatments are explained in the captionof Figure 4. Lifespan during the experiment for thecontrol group is represented by the vertical bar ± SEM (grey area). In barhistograms, the causes of mortality before the grey area are detailed incomparison to the controls (0). In black are the necessary euthanasia becauseof suffering in accordance with ethical rules (tumors over 25% body weight,more than 25% weight loss, hemorrhagic bleeding, etc.); and in hatched areas,spontaneous mortality."<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Muller-Ford_2004Muller-Ford 20042018-10-13T01:17:02Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Muller-Ford, C. S. (2004). Analysis of dermatoglyphic heritability: A study of phenotypic relationships.<br />
<br />
=Links=<br />
*https://scholarworks.umt.edu/cgi/viewcontent.cgi?article=7428&context=etd<br />
*http://hawaiireedlab.com/pdf/m/muller-ford2004.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Crohn%E2%80%99s_DiseaseCrohn’s Disease2018-10-12T18:09:52Z<p>Floyd: Created page with "*https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901108/"</p>
<hr />
<div>*https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901108/</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Boyle_et_al._2017Boyle et al. 20172018-10-11T22:11:09Z<p>Floyd: /* Notes */</p>
<hr />
<div>=Citation=<br />
Boyle, E. A., Li, Y. I., & Pritchard, J. K. (2017). An expanded view of complex traits: from polygenic to omnigenic. ''Cell'', 169(7), 1177--1186.<br />
<br />
=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0092867417306293<br />
*http://hawaiireedlab.com/pdf/b/boyleetal2017.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
A central goal of genetics is to understand the links between genetic variation and disease. Intuitively, one might expect disease-causing variants to cluster into key pathways that drive disease etiology. But for complex traits, association signals tend to be spread across most of the genome—including near many genes without an obvious connection to disease. We propose that gene regulatory networks are sufficiently interconnected such that all genes expressed in disease-relevant cells are liable to affect the functions of core disease-related genes and that most heritability can be explained by effects on genes outside core pathways. We refer to this hypothesis as an “omnigenic” model.<br />
<br />
=Notes=<br />
This is very well written and starts off by placing it in the broad historical overview of understanding the relationship between genotypes and phenotypes. This emphasizes that the results from GWAS suggest that pleiotropy and genetic heterogeneity are widespread and play a very important role in connecting genotype to phenotype (versus classical views like strict Mendalism, Garrod's one gene one function, and the philosophy of genetic dissection, yet these have been very successful approaches).<br />
<br />
Figure 3 is a very important result and point to make. <br />
<br />
''Simply'' searching for GO enrichment categories in GWAS may be a fundamental mistake. <br />
<br />
This brings to mind a number of questions of the importance for the evolution of traits within and between species, and the authors spend some time discussing this. <br />
<br />
I can't help thinking that associations from population structure might be inflating the genome-wide effect (and no one knows this better than the last author, Pritchard). This is mentioned on p. 1179, P. 3, "the signals are not driven by confounding from population structure". Also, this would be widely distributed regardless of gene expression levels or chromatin context. <br />
<br />
Positive selection on a quantitative phenotype could help distribute the diversity reducing hitchhiking effect over a number of loci, smoothing out the correlation between diversity and rates of recombination seen across the genome of some species ([[Begun and Aquadro 1992]], [[Stephan 2010]]). <br />
<br />
I can't help wondering if there could be room for "selfish" allele evolution as a quantitative trait. This is in contrast to most of the thinking I have seen; that selfish alleles must assemble together on a haplotype with suppressed recombination (such as the mouse ''t''-haplotype, [[Silver 1993]]). Otherwise they recombine away from each other and are loose their collective advantage. However, the association of alleles in linkage disequilibrium takes multiple generations to approach equilibrium, even for unlinked freely recombining loci. <br />
<br />
<math>D_g \approx D_0 e^{-g/2}</math>, where ''g'' is generation and ''D'' is the disequilibrium parameter. Approximately 39% of the association is lost per generation, so selection would have to overcome that by removing the recombinant types. <br />
<br />
Some unlinked regions in natural populations appear to be in persistent LD ([[Turner et al. 2005]]; [[Hohenlohe et al. 2012]]). Perhaps these could be candidates for selfish allele evolution, particularly if they are associated with reproduction ([[Turner et al. 2005]]). Also, switching between strategies by independent assortment can enhance some types of fitness interactions (and these might be inhibited by increased linkage, [[Reed 2007]]). Even though they are thought of as selfish, multiple alleles acting together to promote their own survival could be seen as an example of the evolution of cooperation. How much of our complex genetic networks, especially those related to gametogenesis and early embryonic development, might be a by product of selfish allele evolution? Also, here is an example of selection driven in-phase coupling of smaller effects despite recombination (https://onlinelibrary.wiley.com/doi/full/10.1111/j.1558-5646.2009.00622.x ). I need to do a literature search and perhaps some simulation of multilocus freely recombining selfish interactions to see if they could evolve. <br />
<br />
...to be continued. <br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Whyard_et_al._2015Whyard et al. 20152018-10-11T05:45:44Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Whyard, S., Erdelyan, C. N., Partridge, A. L., Singh, A. D., Beebe, N. W., & Capina, R. (2015). Silencing the buzz: a new approach to population suppression of mosquitoes by feeding larvae double-stranded RNAs. Parasites & Vectors, 8(1), 96.<br />
<br />
=Links=<br />
*https://parasitesandvectors.biomedcentral.com/articles/10.1186/s13071-015-0716-6<br />
*http://hawaiireedlab.com/pdf/w/whyardetal2015.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Sterile_Insect_TechniqueSterile Insect Technique2018-10-11T05:42:52Z<p>Floyd: Created page with "=Notes= *Whyard et al. 2015"</p>
<hr />
<div>=Notes=<br />
*[[Whyard et al. 2015]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Ewens_2008Ewens 20082018-10-10T22:50:35Z<p>Floyd: /* Links */</p>
<hr />
<div>Ewens, W. J. (2008) Commentary: On Haldane's ‘defense of beanbag genetics’. International Journal of Epidemiology, 37(3), 447–451. <br />
<br />
=Links=<br />
*https://academic.oup.com/ije/article/37/3/447/747072<br />
*http://hawaiireedlab.com/pdf/e/ewens2008.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Hessel_et_al._2012Hessel et al. 20122018-10-10T01:58:44Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Hessel, A., Goodman, M., & Kotler, S. (2012). Hacking the President’s DNA. The Atlantic, 310(4), 83.<br />
<br />
=Links=<br />
*https://www.theatlantic.com/magazine/archive/2012/11/hacking-the-presidents-dna/309147/<br />
*http://hawaiireedlab.com/pdf/h/hesseletal2012.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Hatemi_et_al._2011Hatemi et al. 20112018-10-09T05:02:42Z<p>Floyd: Created page with "=Citation= Hatemi, P. K., Gillespie, N. A., Eaves, L. J., Maher, B. S., Webb, B. T., Heath, A. C., ... & Montgomery, G. W. (2011). A genome-wide analysis of liberal and conser..."</p>
<hr />
<div>=Citation=<br />
Hatemi, P. K., Gillespie, N. A., Eaves, L. J., Maher, B. S., Webb, B. T., Heath, A. C., ... & Montgomery, G. W. (2011). A genome-wide analysis of liberal and conservative political attitudes. The Journal of Politics, 73(1), 271-285.<br />
<br />
=Links=<br />
*https://www.journals.uchicago.edu/doi/abs/10.1017/S0022381610001015<br />
*http://hawaiireedlab.com/pdf/h/hatemietal2011.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
The assumption that the transmission of social behaviors and political preferences is purely cultural has been challenged repeatedly over the last 40 years by the combined evidence of large studies of adult twins and their relatives, adoption studies, and twins reared apart. Variance components and path modeling analyses using data from extended families quantified the overall genetic influence on political attitudes, but few studies have attempted to localize the parts of the genome which accounted for the heritability estimates found for political preferences. Here, we present the first genome-wide analysis of Conservative-Liberal attitudes from a sample of 13,000 respondents whose DNA was collected in conjunction with a 50-item sociopolitical attitude questionnaire. Several significant linkage peaks were identified and potential candidate genes discussed.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Provine_1991Provine 19912018-10-08T06:17:09Z<p>Floyd: Created page with "=Citation= Provine, W. B. (1991). Alfred Henry Sturtevant and crosses between Drosophila melanogaster and Drosophila simulans. Genetics, 129(1), 1. =Links= *https://www.ncbi...."</p>
<hr />
<div>=Citation=<br />
Provine, W. B. (1991). Alfred Henry Sturtevant and crosses between Drosophila melanogaster and Drosophila simulans. Genetics, 129(1), 1.<br />
<br />
=Links=<br />
*https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1204558/<br />
*http://hawaiireedlab.com/pdf/p/provine1991.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Lombardo_2003Lombardo 20032018-10-08T06:10:07Z<p>Floyd: Created page with "=Citation= Lombardo, P. A. (2003). Facing Carrie Buck. Hastings Center Report, 33(2), 14-17. =Links= *https://onlinelibrary.wiley.com/doi/abs/10.2307/3528148 *http://hawaiire..."</p>
<hr />
<div>=Citation=<br />
Lombardo, P. A. (2003). Facing Carrie Buck. Hastings Center Report, 33(2), 14-17.<br />
<br />
=Links=<br />
*https://onlinelibrary.wiley.com/doi/abs/10.2307/3528148<br />
*http://hawaiireedlab.com/pdf/l/lombardo2003.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Gould_1984Gould 19842018-10-08T06:01:15Z<p>Floyd: Created page with "=Citation= Gould, S. J., (1984) Carrie Buck’s Daughter. ''Natural History'', July. =Links= *https://scholar.google.com/scholar?cluster=7443623301817345558 *http://hawaiiree..."</p>
<hr />
<div>=Citation=<br />
Gould, S. J., (1984) Carrie Buck’s Daughter. ''Natural History'', July.<br />
<br />
=Links=<br />
*https://scholar.google.com/scholar?cluster=7443623301817345558<br />
*http://hawaiireedlab.com/pdf/g/gould1984.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Stern_2005Stern 20052018-10-07T19:20:25Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Stern, A. M. (2005). Sterilized in the name of public health: race, immigration, and reproductive control in modern California. American Journal of Public Health, 95(7), 1128-1138.<br />
<br />
=Links=<br />
*https://ajph.aphapublications.org/doi/abs/10.2105/AJPH.2004.041608<br />
*http://hawaiireedlab.com/pdf/s/stern2005.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
In exploring the history of involuntary sterilization in California, I connect the approximately 20 000 operations performed on patients in state institutions between 1909 and 1979 to the federally funded procedures carried out at a Los Angeles County hospital in the early 1970s.<br />
<br />
Highlighting the confluence of factors that facilitated widespread sterilization abuse in the early 1970s, I trace prosterilization arguments predicated on the protection of public health.<br />
<br />
This historical overview raises important questions about the legacy of eugenics in contemporary California and relates the past to recent developments in health care delivery and genetic screening.<br />
<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Paul_1995Paul 19952018-10-07T18:57:39Z<p>Floyd: </p>
<hr />
<div>=Citation=<br />
Paul, D. B. (1995) ''Controlling Human Heredity: 1865 to the Present''. Humanity Books. <br />
<br />
=Links=<br />
*https://books.google.com/books?id=3xibQgAACAAJ<br />
<br />
=Notes=<br />
This book is focused on the US eugenics movement of the early 1900s. It is densely packed with information. <br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=EugenicsEugenics2018-10-07T17:03:39Z<p>Floyd: /* Publications */</p>
<hr />
<div>Many geneticists in the early 1900s promoted eugenics, and eugenic practices were certainly part of the genetics discussion. Here is a quote from Haldane as an example. <br />
<blockquote><br />
"This may be taken as a rough estimate of the price which the species pays for the variability which is probably a prerequisite for evolution. ... In other words, if we could achieve the aim of negative eugenics and abolish all genes (including autosomal recessives, most of which can not even be detected at present) which seriously lower fitness in our present environments, we might expect a gain in fitness of the order of 10 per cent., though this might lower our capacity for evolution in a changed environment."—p. 348, [[Haldane 1937]]<br />
</blockquote><br />
Eugenic practices such as involuntary sterilizations in the United States became widely adopted. This started to fall out of favor after World War II but some laws and practices remained until the 1970s. Several years ago I made a comment about the US eugenics programs in a college genetics class I was teaching and realized most of the students had never heard of it. This surprised me and I decided to include a lecture on the history of eugenics programs and the misconceptions many of the arguments were based on each semester thereafter. It is not easy to talk about. However, in my opinion college educated biology majors should understand how science can be misused and how quickly things can go wrong. This also serves as an illustration of the ways science and society interact. <br />
<blockquote><br />
"The real danger is not that biology changes with society, but that the public expects biology to provide the objective truth apart from social influences. Geneticists and the public should realize that the science of genetics is often closely intertwined with social attitudes and political considerations."—p. 796, [[Provine 1973]]<br />
</blockquote><br />
One semester I had a student thank me after class for talking about the history of eugenics and she told me that her aunt had been involuntarily sterilized in the California campaign. <br />
<br />
In retrospect it is surprising that so many people are not aware of this history. There are also not a lot of sources of solid information about the US eugenics programs (though some excellent sources do exist, which I will attempt to collect below). This is also a criticism I have of many genetics textbooks; they tend to not discuss eugenics or the GMO debate, both of which are important genetics topics for students to understand. <br />
<br />
=Publications=<br />
*[[Paul 1995]] (comprehensive coverage of the US eugenics movement)<br />
*[[Stern 2005]] (focused on eugenics in California)<br />
*[[Provine 1973]] (not about eugenics but relevant to the issues involved)<br />
*[[Gould 1984]] (commentary on the Carrie Buck case in Virginia)<br />
*[[Lombardo 2003]] (also about the Carrie Buck case)</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Provine_1973Provine 19732018-10-07T16:52:03Z<p>Floyd: Created page with "=Citation= Provine, W. B. (1973). Geneticists and the Biology of Race Crossing: Geneticists changed their minds about the biological effects of race crossing. Science, 182(411..."</p>
<hr />
<div>=Citation=<br />
Provine, W. B. (1973). Geneticists and the Biology of Race Crossing: Geneticists changed their minds about the biological effects of race crossing. Science, 182(4114), 790-796.<br />
<br />
=Links=<br />
*http://science.sciencemag.org/content/182/4114/790<br />
*http://hawaiireedlab.com/pdf/p/provine1973.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
Geneticists in England and the United States clearly reversed their published remarks on the effects of race crossing between 1930 and 1950. The reversal occurred in two steps. First came the change in the 1930's from a condemnation of wide race crosses to an agnostic view. The second change, from the agnostic view to the belief that wide race crosses were at worst biologically harmless, took place during and shortly after World War II.<br />
<br />
The entire reversal occurred in the light of little new compelling data from studies of actual human race crosses. The lack of new data is unsurprising. Few geneticists wished to initiate experiments that took three human generations to complete. And controlled race crosses are hard to arrange, even with government grants. What might be more surprising was the willingness of geneticists to make such positive statements about race crossing when they had so little reliable genetic evidence.<br />
<br />
I interviewed or wrote to ten prominent geneticists who worked on human genetics between 1930 and 1950. Not one believed that new evidence on race crossing was the primary reason why geneticists changed their minds about the effects of race crossing. One plausible explanation, that the rise of "population thinking" (44) caused geneticists to change their minds, does not fit the evidence. Castle was no more of a "population" thinker than East, yet they differed radically in their conclusions about race crossing. What, then, did cause geneticists to change their minds?<br />
<br />
Most important was the revulsion of educated people in the United States and England to Nazi race doctrines and their use in justifying extermination of Jews. Few geneticists wanted to argue, as had the Nazis, that biology showed race crossing was harmful. Instead, having witnessed the horrible toll, geneticists naturally wanted to argue that biology showed race crossing was at worst harmless. No racist nation could misuse that conclusion. And geneticists did revise their biology to fit their feelings of revulsion.<br />
<br />
Geneticists' ideas about the related question of hereditary mental differences between races is perhaps undergoing a similar development to that seen earlier in their ideas about race crossing. In 1951, judging from the response to the Unesco second statement on race and comments in genetics literature, most geneticists agreed with Muller that races probably differed in significant average mental traits. By 1969, when Arthur Jensen advocated this view in his controversial article (45), most geneticists who spoke publicly on the issue had adopted an agnostic position. Knowledge of hereditary racial differences in IQ had scarcely changed since 1951, but society had changed considerably in racial attitudes. It will be interesting to see if during the next several decades geneticists will argue, on the basis of little additional evidence, that hereditary mental differences between races do not exist.<br />
<br />
I am not condemning geneticists because social and political factors have influenced their scientific conclusions about race crossing and race differences. It is necessary and natural that changing social attitudes will influence areas of biology where little is known and the conclusions are possibly socially explosive. The real danger is not that biology changes with society, but that the public expects biology to provide the objective truth apart from social influences. Geneticists and the public should realize that the science of genetics is often closely intertwined with social attitudes and political considerations.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Graffin_and_Provine_2007Graffin and Provine 20072018-10-07T04:40:57Z<p>Floyd: Created page with "=Citation= Graffin, G. W., & Provine, W. B. (2007). Evolution, religion and free will. American Scientist, 95(4), 294. =Links= *https://scholar.google.com/scholar?cluster=700..."</p>
<hr />
<div>=Citation=<br />
Graffin, G. W., & Provine, W. B. (2007). Evolution, religion and free will. American Scientist, 95(4), 294.<br />
<br />
=Links=<br />
*https://scholar.google.com/scholar?cluster=7001837419233312817<br />
*http://hawaiireedlab.com/pdf/g/graffinandprovine2007.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Provine_1987Provine 19872018-10-07T04:30:15Z<p>Floyd: Created page with "=Citation= Provine, W. B. (1987) Trial and Error: The American Controversy over Creation and Evolution. Academe, 73(1), 50--52. =Links= *https://www.jstor.org/stable/4024985..."</p>
<hr />
<div>=Citation=<br />
Provine, W. B. (1987) Trial and Error: The American Controversy over Creation and Evolution. Academe, 73(1), 50--52. <br />
<br />
=Links=<br />
*https://www.jstor.org/stable/40249853<br />
*http://hawaiireedlab.com/pdf/p/provine1987.pdf (internal lab link only)<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Provine_1982Provine 19822018-10-07T04:20:40Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Provine, W. B. (1982). Influence of Darwin's Ideas on the Study of Evolution. Bioscience, 32(6), 501-506.<br />
<br />
=Links=<br />
*https://academic.oup.com/bioscience/article-abstract/32/6/501/322457<br />
*http://hawaiireedlab.com/pdf/p/provine1982.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
Darwin's On the Origin of Species convinced the western world of the fact of evolution. His theory of natural selection, however, was received more hesitantly. Ignorance of the mechanism of heredity, difficulties with understanding the nature of variation in natural populations, and lack of evidence contributed to formation of the opposition. Arguments concerning the continuous or, alternatively, the discontinuous nature of evolution have permeated the history of controversy in evolutionary theory.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Provine,_W._B.Provine, W. B.2018-10-07T04:18:28Z<p>Floyd: /* Publications */</p>
<hr />
<div>I knew Dr. Provine when I was a grad. student at Cornell. I didn't always agree with him but I had tremendous respect for his thoughts, ideas, and discussions. <br />
<br />
=Publications=<br />
*[[Provine 1973]]<br />
*[[Provine 1982]]<br />
*[[Provine 1987]]<br />
*[[Provine 1991]]<br />
*[[Graffin and Provine 2007]]<br />
<br />
[[Category:Person]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_and_Aquadro_2006Reed and Aquadro 20062018-10-07T04:00:15Z<p>Floyd: Created page with "=Citation= Reed, F. A., & Aquadro, C. F. (2006). Mutation, selection and the future of human evolution. TRENDS in Genetics, 22(9), 479-484. =Links= *https://www.sciencedirect..."</p>
<hr />
<div>=Citation=<br />
Reed, F. A., & Aquadro, C. F. (2006). Mutation, selection and the future of human evolution. TRENDS in Genetics, 22(9), 479-484.<br />
<br />
=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0168952506002174<br />
*http://hawaiireedlab.com/pdf/r/reedandaquadro2006.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
Several recent analyses provide growing evidence of the influence of positive selection acting in the ancestors of modern humans. Additionally, the best way to explain current fluctuations in neutral variation across the genome is by including negative selection against a high rate of deleterious mutants. We suggest that explaining these predicted high deleterious mutation rates in humans could require the inclusion of additional factors, such as inbreeding and prezygotic selection, in addition to rank-order selection and fitness interactions among mutations. We also suggest that some forms of selection, rather than being relaxed in modern humans, are probably still acting and might intensify in the near future, and make some predictions about the next several millennia of human evolution.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_et_al._2003Reed et al. 20032018-10-07T03:42:15Z<p>Floyd: /* Links */</p>
<hr />
<div>=Citation=<br />
Reed, F. A., Kontanis, E. J., Kennedy, K. A., & Aquadro, C. F. (2003). Brief communication: ancient DNA prospects from Sri Lankan highland dry caves support an emerging global pattern. American Journal of Physical Anthropology, 121(2), 112-116.<br />
<br />
=Links=<br />
*https://onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.10211<br />
*http://hawaiireedlab.com/pdf/r/reedetal2003.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
Recovery of ancient DNA has become an increasingly important tool in elucidating the origins of past populations and their relationships. Unfortunately, many human skeletal remains do not contain original DNA amplifiable by polymerase chain reaction (PCR). Amino‐acid racemization has proven to be a useful predictor of ancient DNA results. We analyzed the relative levels of amino‐acid preservation and racemization of human samples from two highland dry‐cave sites in Sri Lanka, and found that amino‐acid enantiomer ratios were inconsistent with successful authentic DNA recovery. A review of the literature reveals that these results are consistent with a global pattern of poor DNA preservation in the tropics.<br />
<br />
=Notes=<br />
This was one of our explorations into ancient DNA (the [[Hyde Park Mastodon]] and [[KV5]] projects did not result in publications). At the end of the day we only had negative results. However, we salvaged this into a publication by showing it fit a significant global -pattern of negative results. The only frustrating thing was that the review process with the journal was glacially slow so that other publications came out in the meantime reporting the interaction with climate/temperature and ancient DNA preservation, which we had to incorporate and cite in the revision process. <br />
<br />
The print figure is disrupted by a moiré pattern. At some point I will upload the original figure here. <br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_and_Tishkoff_2006bReed and Tishkoff 2006b2018-10-07T03:37:23Z<p>Floyd: </p>
<hr />
<div>=Citation=<br />
Reed, F. A., & Tishkoff, S. A. (2006). African human diversity, origins and migrations. Current Opinion in Genetics & Development, 16(6), 597-605.<br />
<br />
=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S0959437X06002073<br />
*http://hawaiireedlab.com/pdf/r/reedandtishkoff2006b.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
The continent of Africa is thought to be the site of origin of all modern humans and is the more recent origin of millions of African Americans. Although Africa has the highest levels of human genetic diversity both within and between populations, it is under-represented in studies of human genetics. Recent advances have been made in understanding the origins of modern humans within Africa, the rate of adaptations due to positive selection, the routes taken in the first migrations of modern humans out of Africa, and the degree of admixture with archaic populations. Africa is also in dire need of effective medical interventions, and studies of genetic variation in Africans will shed light on the genetic basis of diseases and resistance to infectious diseases. Thus, we have tremendous potential to learn about human variation and evolutionary history and to positively impact human health care from studies of genetic diversity in Africa.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_and_Tishkoff_2006aReed and Tishkoff 2006a2018-10-07T03:33:58Z<p>Floyd: Created page with "=Citation= Reed, F. A., & Tishkoff, S. A. (2006). Positive selection can create false hotspots of recombination. Genetics, 172(3), 2011-2014. =Links= *http://www.genetics.org..."</p>
<hr />
<div>=Citation=<br />
Reed, F. A., & Tishkoff, S. A. (2006). Positive selection can create false hotspots of recombination. Genetics, 172(3), 2011-2014.<br />
<br />
=Links=<br />
*http://www.genetics.org/content/172/3/2011.short<br />
*http://hawaiireedlab.com/pdf/r/reedandtishkoff2006a.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
Simulations of positive directional selection, under parameter values appropriate for approximating human genetic diversity and rates of recombination, reveal that the effects of strong selective sweeps on patterns of linkage disequilibrium (LD) mimic the pattern expected with recombinant hotspots.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_et_al._2005bReed et al. 2005b2018-10-07T03:27:08Z<p>Floyd: </p>
<hr />
<div>=Citation=<br />
Reed, F. A., Reeves, R. G., & Aquadro, C. F. (2005). Evidence of susceptibility and resistance to cryptic X‐linked meiotic drive in natural populations of Drosophila melanogaster. Evolution, 59(6), 1280-1291.<br />
<br />
=Links=<br />
*https://onlinelibrary.wiley.com/doi/abs/10.1111/j.0014-3820.2005.tb01778.x<br />
*http://hawaiireedlab.com/pdf/r/reedetal2005b.pdf (internal lab link only)<br />
<br />
=Published Abstract=<br />
There is mounting evidence consistent with a general role of positive selection acting on the Drosophila melanogaster X‐chromosome. However, this positive selection need not necessarily arise from forces that are adaptive to the organism. Nonadaptive meiotic drive may exist on the X‐chromosome and contribute to forces of selection. Females from a reference D. melanogaster line, containing the X‐linked marker white, were crossed to males from 49 isofemale lines established from seven African and five non‐African natural populations to detect naturally occurring meiotic drive. Several lines exhibited a departure from expected Mendelian transmission of X‐chromosomes to the third generation (F2) offspring, particularly those from hybrid African male parents. F2 viability was not correlated with skewed chromosomal inheritance. However, a significant difference in viability between cosmopolitan and tropical African crosses was observed. Recombination analysis supports the presence of a male‐acting meiotic drive element near the centromeric region of the X‐chromosome and putative recessive autosomal drive suppression. There is also evidence of another female‐acting drive element linked to white. The possible role meiotic drive may contribute in shaping levels of genetic variation in D. melanogaster, and additional ways to test this hypothesis are discussed.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Gould_et_al._2008Gould et al. 20082018-10-06T22:07:08Z<p>Floyd: </p>
<hr />
<div>=Citation=<br />
Gould, F., Huang, Y., Legros, M., & Lloyd, A. L. (2008). A Killer–Rescue system for self-limiting gene drive of anti-pathogen constructs. Proceedings of the Royal Society of London B: Biological Sciences, 275(1653), 2823-2829.<br />
<br />
=Links=<br />
*http://rspb.royalsocietypublishing.org/content/275/1653/2823.short<br />
<br />
=Published Abstract=<br />
A number of genetic mechanisms have been suggested for driving anti-pathogen genes into natural populations. Each of these mechanisms requires complex genetic engineering, and most are theoretically expected to permanently spread throughout the target species' geographical range. In the near term, risk issues and technical limits of molecular methods could delay the development and use of these mechanisms. We propose a gene-drive mechanism that can be self-limiting over time and space, and is simpler to build. This mechanism involves one gene that codes for toxicity (killer) and a second that confers immunity to the toxic effects (rescue). We use population-genetic models to explore cases with one or two independent insertions of the killer gene and one insertion of the rescue gene. We vary the dominance and penetrance of gene action, as well as the magnitude of fitness costs. Even with the fitness costs of 10 per cent for each gene, the proportion of mosquitoes expected to transmit the pathogen decreases below 5 per cent for over 40 generations after one 2 : 1 release (engineered : wild) or after four 1 : 2 releases. Both the killer and rescue genes will be lost from the population over time, if the rescue construct has any associated fitness cost. Molecular approaches for constructing strains are discussed.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Emerson_et_al._2017Emerson et al. 20172018-10-06T21:16:04Z<p>Floyd: Created page with "=Citation= Emerson, C., James, S., Littler, K., & Randazzo, F. F. (2017). Principles for gene drive research. Science, 358(6367), 1135-1136. =Links= *http://science.sciencema..."</p>
<hr />
<div>=Citation=<br />
Emerson, C., James, S., Littler, K., & Randazzo, F. F. (2017). Principles for gene drive research. Science, 358(6367), 1135-1136.<br />
<br />
=Links=<br />
*http://science.sciencemag.org/content/358/6367/1135.full<br />
<br />
=Published Abstract=<br />
The recent outbreak of Zika virus in the Americas renewed attention on the importance of vector-control strategies to fight the many vector-borne diseases that continue to inflict suffering around the world. In 2015, there were ∼212 million infections and a death every minute from malaria alone (1). Gene drive technology is being explored as a potentially durable and cost-effective strategy for controlling the transmission of deadly and debilitating vector-borne diseases that affect millions of people worldwide, such as Zika virus and malaria. Additionally, its suitability is being evaluated for various potential applications in conservation biology, including a highly specific and humane method for eliminating invasive species from sensitive ecosystems (2, 3).<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Reed_2017Reed 20172018-10-06T21:13:30Z<p>Floyd: Created page with "=Citation= Reed, F. A. (2017). Evolutionary Genetic Engineering in the Indo-Pacific: Conservation, Humanitarian, and Social Issues. arXiv preprint arXiv:1706.01710. =Link= *h..."</p>
<hr />
<div>=Citation=<br />
Reed, F. A. (2017). Evolutionary Genetic Engineering in the Indo-Pacific: Conservation, Humanitarian, and Social Issues. arXiv preprint arXiv:1706.01710.<br />
<br />
=Link=<br />
*https://arxiv.org/abs/1706.01710<br />
<br />
=Published Abstract=<br />
The Indo-Pacific region contains a unique mix of opportunities for the development and use of genetic-pest-management, gene-drive, and gene-drive-like technologies. Here I collectively refer to these technologies as Evolutionary Genetic Engineering (EGE). Indo-Pacific Islands have some of the world's highest rates of endemism and extinction---species and entire ecosystems are at risk. This threat to the natural world is coupled with the burden of human diseases, many of which are new and emerging or neglected tropical diseases. The same factors which have led to high rates of endemism also, in some ways, make this region an ideal testing ground for some types of EGE's. There is great potential for positive humanitarian, economic, and conservation applications of EGE's. However, these types of new technologies will be initially viewed from the perspective of the recent history of a loss of self determination, issues of social justice, and the testing of new technologies (e.g., biocontrol, agricultural, nuclear) in the Indo-Pacific---a region of the world that is still extensively colonized and controlled by Western Nations. Experience with successes and failures in related technologies suggests a path to move forward---a set of eight recommendations---to maximize the potential payoffs and minimize unintended negative effects of EGE's. <br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=McMeniman_et_al._2009McMeniman et al. 20092018-10-06T21:00:00Z<p>Floyd: Created page with "=Citation= McMeniman, C. J., Lane, R. V., Cass, B. N., Fong, A. W., Sidhu, M., Wang, Y. F., & O'neill, S. L. (2009). Stable introduction of a life-shortening Wolbachia infecti..."</p>
<hr />
<div>=Citation=<br />
McMeniman, C. J., Lane, R. V., Cass, B. N., Fong, A. W., Sidhu, M., Wang, Y. F., & O'neill, S. L. (2009). Stable introduction of a life-shortening Wolbachia infection into the mosquito Aedes aegypti. Science, 323(5910), 141-144.<br />
<br />
=Link=<br />
http://science.sciencemag.org/content/323/5910/141<br />
<br />
=Published Abstract=<br />
Most pathogens require a relatively long period of development in their mosquito vector before they can be transmitted to a new human host; hence, only older insects are of epidemiological importance. The successful transfer of a life-shortening strain of the inherited bacterial symbiont, Wolbachia, into the major mosquito vector of dengue, Aedes aegypti, halved adult life span under laboratory conditions. The association is stable, and the Wolbachia strain is maternally inherited at high frequency. It is capable of inducing complete cytoplasmic incompatibility, which should facilitate its invasion into natural field populations and its persistence over time. Our data suggest that targeting mosquito age with inherited Wolbachia infections may be a viable strategy to reduce the transmission of pathogens such as dengue viruses.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Hansen_et_al._2013Hansen et al. 20132018-10-06T20:55:55Z<p>Floyd: Created page with "=Citation= Hansen, M., Flatt, T., & Aguilaniu, H. (2013). Reproduction, fat metabolism, and life span: what is the connection?. Cell metabolism, 17(1), 10-19. =Links= *https:..."</p>
<hr />
<div>=Citation=<br />
Hansen, M., Flatt, T., & Aguilaniu, H. (2013). Reproduction, fat metabolism, and life span: what is the connection?. Cell metabolism, 17(1), 10-19.<br />
<br />
=Links=<br />
*https://www.sciencedirect.com/science/article/pii/S1550413112004949<br />
<br />
=Published Abstract=<br />
Reduced reproduction is associated with increased fat storage and prolonged life span in multiple organisms, but the underlying regulatory mechanisms remain poorly understood. Recent studies in several species provide evidence that reproduction, fat metabolism, and longevity are directly coupled. For instance, germline removal in the nematode Caenorhabditis elegans promotes longevity in part by modulating lipid metabolism through effects on fatty acid desaturation, lipolysis, and autophagy. Here, we review these recent studies and discuss the mechanisms by which reproduction modulates fat metabolism and life span. Elucidating the relationship between these processes could contribute to our understanding of age-related diseases including metabolic disorders.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Yoshida_et_al._2007Yoshida et al. 20072018-10-06T20:47:03Z<p>Floyd: Created page with "=Citation= Yoshida, S., Shimada, Y., Kondoh, D., Kouzuma, Y., Ghosh, A. K., Jacobs-Lorena, M., & Sinden, R. E. (2007). Hemolytic C-type lectin CEL-III from sea cucumber expres..."</p>
<hr />
<div>=Citation=<br />
Yoshida, S., Shimada, Y., Kondoh, D., Kouzuma, Y., Ghosh, A. K., Jacobs-Lorena, M., & Sinden, R. E. (2007). Hemolytic C-type lectin CEL-III from sea cucumber expressed in transgenic mosquitoes impairs malaria parasite development. PLoS Pathogens, 3(12), e192.<br />
<br />
=Link=<br />
*https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.0030192<br />
<br />
=Published Abstract=<br />
The midgut environment of anopheline mosquitoes plays an important role in the development of the malaria parasite. Using genetic manipulation of anopheline mosquitoes to change the environment in the mosquito midgut may inhibit development of the malaria parasite, thus blocking malaria transmission. Here we generate transgenic Anopheles stephensi mosquitoes that express the C-type lectin CEL-III from the sea cucumber, Cucumaria echinata, in a midgut-specific manner. CEL-III has strong and rapid hemolytic activity toward human and rat erythrocytes in the presence of serum. Importantly, CEL-III binds to ookinetes, leading to strong inhibition of ookinete formation in vitro with an IC50 of 15 nM. Thus, CEL-III exhibits not only hemolytic activity but also cytotoxicity toward ookinetes. In these transgenic mosquitoes, sporogonic development of Plasmodium berghei is severely impaired. Moderate, but significant inhibition was found against Plasmodium falciparum. To our knowledge, this is the first demonstration of stably engineered anophelines that affect the Plasmodium transmission dynamics of human malaria. Although our laboratory-based research does not have immediate applications to block natural malaria transmission, these findings have significant implications for the generation of refractory mosquitoes to all species of human Plasmodium and elucidation of mosquito–parasite interactions.<br />
<br />
[[Category:Publication]]</div>Floydhttp://hawaiireedlab.com/labwiki/index.php?title=Moreira_et_al._2002Moreira et al. 20022018-10-06T20:44:40Z<p>Floyd: Created page with "=Citation= Moreira, L. A., Ito, J., Ghosh, A., Devenport, M., Zieler, H., Abraham, E. G., ... & Jacobs-Lorena, M. (2002). Bee venom phospholipase inhibits malaria parasite dev..."</p>
<hr />
<div>=Citation=<br />
Moreira, L. A., Ito, J., Ghosh, A., Devenport, M., Zieler, H., Abraham, E. G., ... & Jacobs-Lorena, M. (2002). Bee venom phospholipase inhibits malaria parasite development in transgenic mosquitoes. Journal of Biological Chemistry, 277(43), 40839-40843.<br />
<br />
=Links=<br />
*http://www.jbc.org/content/277/43/40839.short<br />
<br />
=Published Abstract=<br />
Malaria kills millions of people every year, and new control measures are urgently needed. The recent demonstration that (effector) genes can be introduced into the mosquito germ line to diminish their ability to transmit the malaria parasite offers new hope toward the fight of the disease (Ito, J., Ghosh, A., Moreira, L. A., Wimmer, E. A. & Jacobs-Lorena, M. (2002)Nature, 417, 452–455). Because of the high selection pressure that an effector gene imposes on the parasite population, development of resistant strains is likely to occur. In search of additional antiparasitic effector genes, we have generated transgenicAnopheles stephensi mosquitoes that express the bee venom phospholipase A2 (PLA2) gene from the gut-specific and blood-inducible Anopheles gambiaecarboxypeptidase (AgCP) promoter. Northern blot analysis indicated that the PLA2 mRNA is specifically expressed in the guts of transgenic mosquitoes with peak expression at ∼4 h after blood ingestion. Western blot and immunofluorescence analyses detected PLA2 protein in the midgut epithelia of transgenic mosquitoes from 8 to 24 h after a blood meal. Importantly, transgene expression reducedPlasmodium berghei oocyst formation by 87% on average and greatly impaired transmission of the parasite to naive mice. The results indicate that PLA2 may be used as an additional effector gene to block the development of the malaria parasite in mosquitoes. <br />
<br />
[[Category:Publication]]</div>Floyd