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  • 1
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    Genetic dissection of transcriptional regulation in budding yeast (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-30
    Description: To begin to understand the genetic architecture of natural variation in gene expression, we carried out genetic linkage analysis of genomewide expression patterns in a cross between a laboratory strain and a wild strain of Saccharomyces cerevisiae. Over 1500 genes were differentially expressed between the parent strains. Expression levels of 570 genes were linked to one or more different loci, with most expression levels showing complex inheritance patterns. The loci detected by linkage fell largely into two categories: cis-acting modulators of single genes and trans-acting modulators of many genes. We found eight such trans-acting loci, each affecting the expression of a group of 7 to 94 genes of related function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brem, Rachel B -- Yvert, Gael -- Clinton, Rebecca -- Kruglyak, Leonid -- GM64268/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):752-5. Epub 2002 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fred Hutchinson Cancer Research Center (FHCRC), 1100 Fairview Avenue North, D4-100, Seattle, WA 98109, USA and Howard Hughes Medical Institute.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923494" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; Crosses, Genetic ; *DNA-Binding Proteins ; Fungal Proteins/genetics/metabolism ; Gene Expression Profiling ; *Gene Expression Regulation, Fungal ; Genes, Fungal ; Genetic Linkage ; Genetic Markers ; Genome, Fungal ; Genotype ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Genetic ; RNA, Fungal/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Regulatory Sequences, Nucleic Acid ; Saccharomyces cerevisiae/*genetics/growth & development/physiology ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Trans-Activators/genetics/metabolism ; Transcription Factors/genetics/metabolism ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Large-scale identification, mapping, and genotyping of single-nucleotide polymorphisms in the human genome (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: Single-nucleotide polymorphisms (SNPs) are the most frequent type of variation in the human genome, and they provide powerful tools for a variety of medical genetic studies. In a large-scale survey for SNPs, 2.3 megabases of human genomic DNA was examined by a combination of gel-based sequencing and high-density variation-detection DNA chips. A total of 3241 candidate SNPs were identified. A genetic map was constructed showing the location of 2227 of these SNPs. Prototype genotyping chips were developed that allow simultaneous genotyping of 500 SNPs. The results provide a characterization of human diversity at the nucleotide level and demonstrate the feasibility of large-scale identification of human SNPs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, D G -- Fan, J B -- Siao, C J -- Berno, A -- Young, P -- Sapolsky, R -- Ghandour, G -- Perkins, N -- Winchester, E -- Spencer, J -- Kruglyak, L -- Stein, L -- Hsie, L -- Topaloglou, T -- Hubbell, E -- Robinson, E -- Mittmann, M -- Morris, M S -- Shen, N -- Kilburn, D -- Rioux, J -- Nusbaum, C -- Rozen, S -- Hudson, T J -- Lipshutz, R -- Chee, M -- Lander, E S -- HG00098/HG/NHGRI NIH HHS/ -- HG01323/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 15;280(5366):1077-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582121" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alleles ; Chromosome Mapping/*methods ; DNA, Complementary ; Databases, Factual ; Deoxyribonucleotides/*genetics ; Dinucleoside Phosphates ; Gene Expression ; Genetic Markers ; *Genetic Techniques ; Genetic Variation ; *Genome, Human ; *Genotype ; Heterozygote ; Homozygote ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Tagged Sites
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Molecular basis of the copulatory plug polymorphism in Caenorhabditis elegans (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-18
    Description: Heritable variation is the raw material for evolutionary change, and understanding its genetic basis is one of the central problems in modern biology. We investigated the genetic basis of a classic phenotypic dimorphism in the nematode Caenorhabditis elegans. Males from many natural isolates deposit a copulatory plug after mating, whereas males from other natural isolates?including the standard wild-type strain (N2 Bristol) that is used in most research laboratories?do not deposit plugs. The copulatory plug is a gelatinous mass that covers the hermaphrodite vulva, and its deposition decreases the mating success of subsequent males. We show that the plugging polymorphism results from the insertion of a retrotransposon into an exon of a novel mucin-like gene, plg-1, whose product is a major structural component of the copulatory plug. The gene is expressed in a subset of secretory cells of the male somatic gonad, and its loss has no evident effects beyond the loss of male mate-guarding. Although C. elegans descends from an obligate-outcrossing, male?female ancestor, it occurs primarily as self-fertilizing hermaphrodites. The reduced selection on male?male competition associated with the origin of hermaphroditism may have permitted the global spread of a loss-of-function mutation with restricted pleiotropy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597896/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597896/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Palopoli, Michael F -- Rockman, Matthew V -- TinMaung, Aye -- Ramsay, Camden -- Curwen, Stephen -- Aduna, Andrea -- Laurita, Jason -- Kruglyak, Leonid -- P20 RR-016463/RR/NCRR NIH HHS/ -- P50 GM071508/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Aug 21;454(7207):1019-22. doi: 10.1038/nature07171. Epub 2008 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Bowdoin College, 6500 College Station, Brunswick, Maine 04011, USA. mpalopol@bowdoin.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18633349" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/*genetics/physiology ; Caenorhabditis elegans Proteins/chemistry/*genetics/metabolism ; *Copulation ; Disorders of Sex Development/genetics ; Gene Expression Regulation ; Male ; Mucins/chemistry/*genetics/metabolism ; *Polymorphism, Genetic ; Retroelements/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Comprehensive polymorphism survey elucidates population structure of Saccharomyces cerevisiae (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-02-13
    Description: Comprehensive identification of polymorphisms among individuals within a species is essential both for studying the genetic basis of phenotypic differences and for elucidating the evolutionary history of the species. Large-scale polymorphism surveys have recently been reported for human, mouse and Arabidopsis thaliana. Here we report a nucleotide-level survey of genomic variation in a diverse collection of 63 Saccharomyces cerevisiae strains sampled from different ecological niches (beer, bread, vineyards, immunocompromised individuals, various fermentations and nature) and from locations on different continents. We hybridized genomic DNA from each strain to whole-genome tiling microarrays and detected 1.89 million single nucleotide polymorphisms, which were grouped into 101,343 distinct segregating sites. We also identified 3,985 deletion events of length 〉200 base pairs among the surveyed strains. We analysed the genome-wide patterns of nucleotide polymorphism and deletion variants, and measured the extent of linkage disequilibrium in S. cerevisiae. These results and the polymorphism resource we have generated lay the foundation for genome-wide association studies in yeast. We also examined the population structure of S. cerevisiae, providing support for multiple domestication events as well as insight into the origins of pathogenic strains.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782482/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782482/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schacherer, Joseph -- Shapiro, Joshua A -- Ruderfer, Douglas M -- Kruglyak, Leonid -- GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-059001/GM/NIGMS NIH HHS/ -- P50 GM071508-059002/GM/NIGMS NIH HHS/ -- R37 MH059520/MH/NIMH NIH HHS/ -- R37 MH059520-12/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Mar 19;458(7236):342-5. doi: 10.1038/nature07670. Epub 2009 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics, Department of Ecology and Evolutionary Biology and Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19212320" target="_blank"〉PubMed〈/a〉
    Keywords: Ecosystem ; Genetics, Population ; *Genomics ; Humans ; Linkage Disequilibrium/genetics ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide/*genetics ; Saccharomyces cerevisiae/*classification/*genetics/isolation & purification
    Print ISSN: 0028-0836
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  • 5
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    Finding the missing heritability of complex diseases (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-09
    Description: Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831613/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manolio, Teri A -- Collins, Francis S -- Cox, Nancy J -- Goldstein, David B -- Hindorff, Lucia A -- Hunter, David J -- McCarthy, Mark I -- Ramos, Erin M -- Cardon, Lon R -- Chakravarti, Aravinda -- Cho, Judy H -- Guttmacher, Alan E -- Kong, Augustine -- Kruglyak, Leonid -- Mardis, Elaine -- Rotimi, Charles N -- Slatkin, Montgomery -- Valle, David -- Whittemore, Alice S -- Boehnke, Michael -- Clark, Andrew G -- Eichler, Evan E -- Gibson, Greg -- Haines, Jonathan L -- Mackay, Trudy F C -- McCarroll, Steven A -- Visscher, Peter M -- P50 GM065509/GM/NIGMS NIH HHS/ -- P50 GM065509-080006/GM/NIGMS NIH HHS/ -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 HL072904/HL/NHLBI NIH HHS/ -- R01 HL072904-07/HL/NHLBI NIH HHS/ -- R01 MH084695/MH/NIMH NIH HHS/ -- U01 HL084706/HL/NHLBI NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- England -- Nature. 2009 Oct 8;461(7265):747-53. doi: 10.1038/nature08494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Human Genome Research Institute, Building 31, Room 4B09, 31 Center Drive, MSC 2152, Bethesda, Maryland 20892-2152, USA. manoliot@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19812666" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Diseases, Inborn/*genetics ; Genetic Predisposition to Disease/*genetics ; Genetics, Medical/*methods/trends ; Genome-Wide Association Study/methods/trends ; Humans ; Inheritance Patterns/genetics ; Pedigree
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Dissection of genetically complex traits with extremely large pools of yeast segregants (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-16
    Description: Most heritable traits, including many human diseases, are caused by multiple loci. Studies in both humans and model organisms, such as yeast, have failed to detect a large fraction of the loci that underlie such complex traits. A lack of statistical power to identify multiple loci with small effects is undoubtedly one of the primary reasons for this problem. We have developed a method in yeast that allows the use of much larger sample sizes than previously possible and hence permits the detection of multiple loci with small effects. The method involves generating very large numbers of progeny from a cross between two Saccharomyces cerevisiae strains and then phenotyping and genotyping pools of these offspring. We applied the method to 17 chemical resistance traits and mitochondrial function, and identified loci for each of these phenotypes. We show that the level of genetic complexity underlying these quantitative traits is highly variable, with some traits influenced by one major locus and others by at least 20 loci. Our results provide an empirical demonstration of the genetic complexity of a number of traits and show that it is possible to identify many of the underlying factors using straightforward techniques. Our method should have broad applications in yeast and can be extended to other organisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862354/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ehrenreich, Ian M -- Torabi, Noorossadat -- Jia, Yue -- Kent, Jonathan -- Martis, Stephen -- Shapiro, Joshua A -- Gresham, David -- Caudy, Amy A -- Kruglyak, Leonid -- F32 HG005176/HG/NHGRI NIH HHS/ -- F32 HG005176-01/HG/NHGRI NIH HHS/ -- F32 HG51762/HG/NHGRI NIH HHS/ -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-01/GM/NIGMS NIH HHS/ -- R37 MH059520/MH/NIMH NIH HHS/ -- R37 MH059520-13/MH/NIMH NIH HHS/ -- R37 MH59520/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Apr 15;464(7291):1039-42. doi: 10.1038/nature08923.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, New Jersey 08540, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393561" target="_blank"〉PubMed〈/a〉
    Keywords: 4-Nitroquinoline-1-oxide/pharmacology ; Chromosome Mapping/*methods ; Crosses, Genetic ; Diploidy ; Drug Resistance, Fungal/drug effects/genetics ; Gene Frequency ; Genotype ; Haploidy ; Mitochondria/metabolism ; Multifactorial Inheritance/*genetics ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/*genetics ; Quinolones/pharmacology ; Saccharomyces cerevisiae/cytology/drug effects/*genetics/metabolism ; Sample Size
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Genetics. It's the sequence, stupid! (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-10-18
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765165/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4765165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coller, Hilary A -- Kruglyak, Leonid -- R01 GM081686/GM/NIGMS NIH HHS/ -- R01 GM086465/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):380-1. doi: 10.1126/science.1165664.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA. hcoller@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18927376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human, Pair 21/*genetics/metabolism ; Disease Models, Animal ; Down Syndrome/genetics ; *Gene Expression Regulation ; Hepatocytes/*metabolism ; Histones/metabolism ; Humans ; Mice ; RNA, Messenger/genetics/metabolism ; *Regulatory Sequences, Nucleic Acid ; Species Specificity ; Transcription Factors/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 8
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    A polymorphism in npr-1 is a behavioral determinant of pathogen susceptibility in C. elegans (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-01-20
    Description: The nematode Caenorhabditis elegans responds to pathogenic bacteria with conserved innate immune responses and pathogen avoidance behaviors. We investigated natural variation in C. elegans resistance to pathogen infection. With the use of quantitative genetic analysis, we determined that the pathogen susceptibility difference between the laboratory wild-type strain N2 and the wild isolate CB4856 is caused by a polymorphism in the npr-1 gene, which encodes a homolog of the mammalian neuropeptide Y receptor. We show that the mechanism of NPR-1-mediated pathogen resistance is through oxygen-dependent behavioral avoidance rather than direct regulation of innate immunity. For C. elegans, bacteria represent food but also a potential source of infection. Our data underscore the importance of behavioral responses to oxygen levels in finding an optimal balance between these potentially conflicting cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748219/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748219/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, Kirthi C -- Andersen, Erik C -- Kruglyak, Leonid -- Kim, Dennis H -- GM071508/GM/NIGMS NIH HHS/ -- GM084477/GM/NIGMS NIH HHS/ -- HG004321/HG/NHGRI NIH HHS/ -- R01 GM084477/GM/NIGMS NIH HHS/ -- R01 GM084477-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-02/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):382-4. doi: 10.1126/science.1166527.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Caenorhabditis elegans/*genetics/immunology/*microbiology/physiology ; Caenorhabditis elegans Proteins/*genetics/*physiology ; Cues ; Genes, Helminth ; Immunity, Innate ; Movement ; Mutation ; Oxygen/physiology ; Polymorphism, Genetic ; Pseudomonas aeruginosa/*pathogenicity/physiology ; Receptors, Neuropeptide Y/*genetics/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Selection at linked sites shapes heritable phenotypic variation in C. elegans (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-16
    Description: Mutation generates the heritable variation that genetic drift and natural selection shape. In classical quantitative genetic models, drift is a function of the effective population size and acts uniformly across traits, whereas mutation and selection act trait-specifically. We identified thousands of quantitative trait loci (QTLs) influencing transcript abundance traits in a cross of two Caenorhabditis elegans strains; although trait-specific mutation and selection explained some of the observed pattern of QTL distribution, the pattern was better explained by trait-independent variation in the intensity of selection on linked sites. Our results suggest that traits in C. elegans exhibit different levels of variation less because of their own attributes than because of differences in the effective population sizes of the genomic regions harboring their underlying loci.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138179/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rockman, Matthew V -- Skrovanek, Sonja S -- Kruglyak, Leonid -- P50 GM071508/GM/NIGMS NIH HHS/ -- P50 GM071508-01/GM/NIGMS NIH HHS/ -- R01 GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-01/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Oct 15;330(6002):372-6. doi: 10.1126/science.1194208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology and Center for Genomics and Systems Biology, New York University, 100 Washington Square East, New York, NY 10003, USA. mrockman@nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20947766" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Caenorhabditis elegans/*genetics/physiology ; Chromosome Mapping ; Chromosomes/*genetics ; Crosses, Genetic ; Evolution, Molecular ; Gene Expression ; Genes, Helminth ; *Genetic Variation ; Logistic Models ; Models, Genetic ; Mutation ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Polymorphism, Single Nucleotide ; Population Density ; *Quantitative Trait Loci ; *Quantitative Trait, Heritable ; Recombination, Genetic ; *Selection, Genetic
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  • 10
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    Natural variation in a chloride channel subunit confers avermectin resistance in C. elegans (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-04
    Description: Resistance of nematodes to anthelmintics such as avermectins has emerged as a major global health and agricultural problem, but genes conferring natural resistance to avermectins are unknown. We show that a naturally occurring four-amino-acid deletion in the ligand-binding domain of GLC-1, the alpha-subunit of a glutamate-gated chloride channel, confers resistance to avermectins in the model nematode Caenorhabditis elegans. We also find that the same variant confers resistance to the avermectin-producing bacterium Streptomyces avermitilis. Population-genetic analyses identified two highly divergent haplotypes at the glc-1 locus that have been maintained at intermediate frequencies by long-term balancing selection. These results implicate variation in glutamate-gated chloride channels in avermectin resistance and provide a mechanism by which such resistance can be maintained.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273849/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghosh, Rajarshi -- Andersen, Erik C -- Shapiro, Joshua A -- Gerke, Justin P -- Kruglyak, Leonid -- P50-GM071508/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- R01 HG004321-03/HG/NHGRI NIH HHS/ -- R01-HG004321/HG/NHGRI NIH HHS/ -- R37- MH59520/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Feb 3;335(6068):574-8. doi: 10.1126/science.1214318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lewis-Sigler Institute for Integrative Genomics, Department of Ecology and Evolutionary Biology, and Howard Hughes Medical Institute, Princeton University, Princeton, NJ 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22301316" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Antinematodal Agents/*pharmacology ; Caenorhabditis elegans/*drug effects/*genetics/physiology ; Caenorhabditis elegans Proteins/chemistry/*genetics/metabolism ; Chloride Channels/chemistry/*genetics/metabolism ; Crosses, Genetic ; Drug Resistance/genetics ; Genes, Helminth ; Genome-Wide Association Study ; Ivermectin/*analogs & derivatives/*pharmacology ; Ligands ; Molecular Sequence Data ; Mutation ; Polymorphism, Single Nucleotide ; Protein Structure, Tertiary ; Quantitative Trait Loci ; Selection, Genetic ; Streptomyces/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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