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156. Systems genetics of sensation seeking

Author

Dickson, Price E., primary, Roy, Tyler A., additional, McNaughton, Kathryn A., additional, Wilcox, Troy D., additional, Kumar, Padam, additional, and Chesler, Elissa J., additional

Published
2018
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157. Genetic mapping in Diversity Outbred mice identifies aTrpa1variant influencing late phase formalin response

Author

Recla, Jill M., primary, Bubier, Jason A., additional, Gatti, Daniel M., additional, Ryan, Jennifer L., additional, Long, Katie H., additional, Robledo, Raymond F., additional, Glidden, Nicole, additional, Hou, Guoqiang, additional, Churchill, Gary A., additional, Maser, Richard S., additional, Zhang, Zhong-wei, additional, Young, Erin E., additional, Chesler, Elissa J., additional, and Bult, Carol J., additional

Published
2018
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158. Systems genetic discovery of host-microbiome interactions reveals mechanisms of microbial involvement in disease

Author

Bubier, Jason A., primary, Philip, Vivek M., additional, Quince, Christopher, additional, Campbell, James, additional, Zhou, Yanjiao, additional, Vishnivetskaya, Tatiana, additional, Duvvuru, Suman, additional, Blair, Rachel Hageman, additional, Ndukum, Juliet, additional, Donohue, Kevin D., additional, Phillips, Charles, additional, Foster, Carmen M., additional, Mellert, David J., additional, Weinstock, George, additional, Culiat, Cymbeline T., additional, Baker, Erich J., additional, Langston, Michael A., additional, O’Hara, Bruce, additional, Palumbo, Anthony V., additional, Podar, Mircea, additional, and Chesler, Elissa J., additional

Published
2018
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160. Reproducibility and replicability of rodent phenotyping in preclinical studies

Author

Kafkafi, Neri, primary, Agassi, Joseph, additional, Chesler, Elissa J., additional, Crabbe, John C., additional, Crusio, Wim E., additional, Eilam, David, additional, Gerlai, Robert, additional, Golani, Ilan, additional, Gomez-Marin, Alex, additional, Heller, Ruth, additional, Iraqi, Fuad, additional, Jaljuli, Iman, additional, Karp, Natasha A., additional, Morgan, Hugh, additional, Nicholson, George, additional, Pfaff, Donald W., additional, Richter, S. Helene, additional, Stark, Philip B., additional, Stiedl, Oliver, additional, Stodden, Victoria, additional, Tarantino, Lisa M., additional, Tucci, Valter, additional, Valdar, William, additional, Williams, Robert W., additional, Würbel, Hanno, additional, and Benjamini, Yoav, additional

Published
2018
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161. Identification of Quantitative Trait Loci and Candidate Genes for an Anxiolytic-like Response to Ethanol in BXD Recombinant Inbred Strains

Author

Putman, Alexander H., Wolen, Aaron R., Harenza, JoLynne, Yordanova, Roumyana K., Webb, Bradley T., Chesler, Elissa J., and Miles, Michael F.

Subjects
Male, Mice, Alcohol Drinking, Anti-Anxiety Agents, Ethanol, Quantitative Trait Loci, Animals, Chromosome Mapping, Genetic Variation, Alcohol-Related Disorders, Article, Genetic Association Studies
Abstract

Genetic differences in acute behavioral responses to ethanol contribute to the susceptibility to alcohol use disorder and the reduction of anxiety is a commonly reported motive underlying ethanol consumption among alcoholics. Therefore, we studied the genetic variance in anxiolytic-like responses to ethanol across the BXD recombinant inbred (RI) mouse panel using the light-dark transition model of anxiety. Strain-mean genetic mapping and a mixed-model quantitative trait loci (QTL) analysis replicated several previously published QTL for locomotor activity and identified several novel anxiety-related loci. Significant loci included a chromosome 11 saline anxiety-like QTL (Salanq1) and a chromosome 12 locus (Etanq1) influencing the anxiolytic-like response to ethanol. Etanq1 was successfully validated by studies with BXD advanced intercross strains and fine-mapped to a region comprising less than 3.5 Mb. Through integration of genome-wide mRNA expression profiles of the mesocorticolimbic reward circuit (prefrontal cortex, nucleus accumbens and ventral midbrain) across the BXD RI panel, we identified high priority candidate genes within Etanq1, the strongest of which was Ninein (Nin), a Gsk3β-interacting protein that is highly expressed in the brain.

Published
2016

162. Identification of a novel gene regulating amygdala-mediated fear extinction

Author

Gunduz-Cinar, Ozge, primary, Brockway, Emma, additional, Lederle, Lauren, additional, Wilcox, Troy, additional, Halladay, Lindsay R., additional, Ding, Ying, additional, Oh, Hyunjung, additional, Busch, Erica F., additional, Kaugars, Katie, additional, Flynn, Shaun, additional, Limoges, Aaron, additional, Bukalo, Olena, additional, MacPherson, Kathryn P., additional, Masneuf, Sophie, additional, Pinard, Courtney, additional, Sibille, Etienne, additional, Chesler, Elissa J., additional, and Holmes, Andrew, additional

Published
2018
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163. Large-scale discovery of mouse transgenic integration sites reveals frequent structural variation and insertional mutagenesis

Author

Goodwin, Leslie O., primary, Splinter, Erik, additional, Davis, Tiffany L., additional, Urban, Rachel, additional, He, Hao, additional, Braun, Robert E., additional, Chesler, Elissa J., additional, Kumar, Vivek, additional, van Min, Max, additional, Ndukum, Juliet, additional, Philip, Vivek M., additional, Reinholdt, Laura G., additional, Svenson, Karen, additional, White, Jacqueline K., additional, Sasner, Michael, additional, Lutz, Cathleen, additional, and Murray, Stephen A., additional

Published
2017
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164. Mouse Phenome Database: an integrative database and analysis suite for curated empirical phenotype data from laboratory mice

Author

Bogue, Molly A, primary, Grubb, Stephen C, additional, Walton, David O, additional, Philip, Vivek M, additional, Kolishovski, Georgi, additional, Stearns, Tim, additional, Dunn, Matthew H, additional, Skelly, Daniel A, additional, Kadakkuzha, Beena, additional, TeHennepe, Gregg, additional, Kunde-Ramamoorthy, Govindarajan, additional, and Chesler, Elissa J, additional

Published
2017
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165. Male Infertility Is Responsible for Nearly Half of the Extinction Observed in the Mouse Collaborative Cross

Author

Shorter, John R, primary, Odet, Fanny, additional, Aylor, David L, additional, Pan, Wenqi, additional, Kao, Chia-Yu, additional, Fu, Chen-Ping, additional, Morgan, Andrew P, additional, Greenstein, Seth, additional, Bell, Timothy A, additional, Stevans, Alicia M, additional, Feathers, Ryan W, additional, Patel, Sunny, additional, Cates, Sarah E, additional, Shaw, Ginger D, additional, Miller, Darla R, additional, Chesler, Elissa J, additional, McMillian, Leonard, additional, O’Brien, Deborah A, additional, and Villena, Fernando Pardo-Manuel de, additional

Published
2017
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168. Aging Research Using Mouse Models

Author

Ackert-Bicknell, Cheryl L., Anderson, Laura, Sheehan, Susan, Hill, Warren G., Chang, Bo, Churchill, Gary A., Chesler, Elissa J., Korstanje, Ron, and Peters, Luanne L.

Subjects
Aging, Disease Models, Animal, Mice, Behavior, Animal, Laboratory Animal Science, Research Design, Longevity, Animal Structures, Animals, Humans, Article
Abstract

Despite the dramatic increase in human lifespan over the past century, there remains pronounced variability in "health-span," or the period of time in which one is generally healthy and free of disease. Much of the variability in health-span and lifespan is thought to be genetic in origin. Understanding the genetic mechanisms of aging and identifying ways to boost longevity is a primary goal in aging research. Here, we describe a pipeline of phenotypic assays for assessing mouse models of aging. This pipeline includes behavior/cognition testing, body composition analysis, and tests of kidney function, hematopoiesis, and immune function, as well as physical parameters. We also describe study design methods for assessing lifespan and health-span, and other important considerations when conducting aging research in the laboratory mouse. The tools and assays provided can assist researchers with understanding the correlative relationships between age-associated phenotypes and, ultimately, the role of specific genes in the aging process.

Published
2015

169. R2d2 drives selfish sweeps in the house mouse

Author

Didion, John P, Morgan, Andrew P, Yadgary, Liran, Bell, Timothy A, McMullan, Rachel C, de Solorzano, Lydia Ortiz, Britton-Davidian, Janice, Bult, Carol J, Campbell, Karl J, Castiglia, Riccardo, Ching, Yung-Hao, Chunco, Amanda J, Crowley, James J, Chesler, Elissa J, Förster, Daniel W, French, John E, Gabriel, Sofia I, Gatti, Daniel M, Garland, Theodore, Giagia-Athanasopoulou, Eva B, Giménez, Mabel D, Grize, Sofia A, Günduz, Islam, Holmes, Andrew, Hauffe, Heidi C, Herman, Jeremy S, Holt, James M, Hua, Kunjie, Jolley, Wesley J, Lindholm, Anna K, Lopez-Fuster, Maria J, Mitsainas, George, da Luz Mathias, Maria, McMillan, Leonard, da Graca Morgado Ramalhinho, Maria, Rehermann, Barbara, Rosshart, Stephan P, Searle, Jeremy B, Shiao, Meng-Shin, Solano, Emanuela, Svenson, Karen L, Thomas-Laemont, Patricia, Threadgill, David W, Ventura, Jacint, Weinstock, George M, Pomp, Daniel, Churchill, Gary A, de Villena, Fernando Pardo-Manuel, Didion, John P, Morgan, Andrew P, Yadgary, Liran, Bell, Timothy A, McMullan, Rachel C, de Solorzano, Lydia Ortiz, Britton-Davidian, Janice, Bult, Carol J, Campbell, Karl J, Castiglia, Riccardo, Ching, Yung-Hao, Chunco, Amanda J, Crowley, James J, Chesler, Elissa J, Förster, Daniel W, French, John E, Gabriel, Sofia I, Gatti, Daniel M, Garland, Theodore, Giagia-Athanasopoulou, Eva B, Giménez, Mabel D, Grize, Sofia A, Günduz, Islam, Holmes, Andrew, Hauffe, Heidi C, Herman, Jeremy S, Holt, James M, Hua, Kunjie, Jolley, Wesley J, Lindholm, Anna K, Lopez-Fuster, Maria J, Mitsainas, George, da Luz Mathias, Maria, McMillan, Leonard, da Graca Morgado Ramalhinho, Maria, Rehermann, Barbara, Rosshart, Stephan P, Searle, Jeremy B, Shiao, Meng-Shin, Solano, Emanuela, Svenson, Karen L, Thomas-Laemont, Patricia, Threadgill, David W, Ventura, Jacint, Weinstock, George M, Pomp, Daniel, Churchill, Gary A, and de Villena, Fernando Pardo-Manuel

Abstract

A selective sweep is the result of strong positive selection driving newly occurring or standing genetic variants to fixation, and can dramatically alter the pattern and distribution of allelic diversity in a population. Population-level sequencing data have enabled discoveries of selective sweeps associated with genes involved in recent adaptations in many species. In contrast, much debate but little evidence addresses whether “selfish” genes are capable of fixation – thereby leaving signatures identical to classical selective sweeps – despite being neutral or deleterious to organismal fitness. We previously described R2d2, a large copy-number variant that causes non-random segregation of mouse Chromosome 2 in females due to meiotic drive. Here we show population-genetic data consistent with a selfish sweep driven by alleles of R2d2 with high copy number (R2d2HC) in natural populations. We replicate this finding in multiple closed breeding populations from six outbred backgrounds segregating for R2d2 alleles. We find that R2d2HC rapidly increases in frequency, and in most cases becomes fixed in significantly fewer generations than can be explained by genetic drift. R2d2HC is also associated with significantly reduced litter sizes in heterozygous mothers, making it a true selfish allele. Our data provide direct evidence of populations actively undergoing selfish sweeps, and demonstrate that meiotic drive can rapidly alter the genomic landscape in favor of mutations with neutral or even negative effects on overall Darwinian fitness. Further study will reveal the incidence of selfish sweeps, and will elucidate the relative contributions of selfish genes, adaptation and genetic drift to evolution.

Published
2016

170. Diversity Outbred Mice at 21: Maintaining Allelic Variation in the Face of Selection

Author

Chesler, Elissa J, primary, Gatti, Daniel M, additional, Morgan, Andrew P, additional, Strobel, Marge, additional, Trepanier, Laura, additional, Oberbeck, Denesa, additional, McWeeney, Shannon, additional, Hitzemann, Robert, additional, Ferris, Martin, additional, McMullan, Rachel, additional, Clayshultle, Amelia, additional, Bell, Timothy A, additional, de Villena, Fernando Pardo-Manuel, additional, and Churchill, Gary A, additional

Published
2016
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172. Reproducibility and replicability of rodent phenotyping in preclinical studies

Author

Kafkafi, Neri, primary, Agassi, Joseph, additional, Chesler, Elissa J., additional, Crabbe, John C., additional, Crusio, Wim E., additional, Eilam, David, additional, Gerlai, Robert, additional, Golani, Ilan, additional, Gomez-Marin, Alex, additional, Heller, Ruth, additional, Iraqi, Fuad, additional, Jaljuli, Iman, additional, Karp, Natasha A., additional, Morgan, Hugh, additional, Nicholson, George, additional, Pfaff, Donald W., additional, Richter, S. Helene, additional, Stark, Philip B., additional, Stiedl, Oliver, additional, Stodden, Victoria, additional, Tarantino, Lisa M., additional, Tucci, Valter, additional, Valdar, William, additional, Williams, Robert W., additional, Würbel, Hanno, additional, and Benjamini, Yoav, additional

Published
2016
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173. R2d2Drives Selfish Sweeps in the House Mouse

Author

Didion, John P., primary, Morgan, Andrew P., additional, Yadgary, Liran, additional, Bell, Timothy A., additional, McMullan, Rachel C., additional, Ortiz de Solorzano, Lydia, additional, Britton-Davidian, Janice, additional, Bult, Carol J., additional, Campbell, Karl J., additional, Castiglia, Riccardo, additional, Ching, Yung-Hao, additional, Chunco, Amanda J., additional, Crowley, James J., additional, Chesler, Elissa J., additional, Förster, Daniel W., additional, French, John E., additional, Gabriel, Sofia I., additional, Gatti, Daniel M., additional, Garland, Theodore, additional, Giagia-Athanasopoulou, Eva B., additional, Giménez, Mabel D., additional, Grize, Sofia A., additional, Gündüz, İslam, additional, Holmes, Andrew, additional, Hauffe, Heidi C., additional, Herman, Jeremy S., additional, Holt, James M., additional, Hua, Kunjie, additional, Jolley, Wesley J., additional, Lindholm, Anna K., additional, López-Fuster, María J., additional, Mitsainas, George, additional, da Luz Mathias, Maria, additional, McMillan, Leonard, additional, Ramalhinho, Maria da Graça Morgado, additional, Rehermann, Barbara, additional, Rosshart, Stephan P., additional, Searle, Jeremy B., additional, Shiao, Meng-Shin, additional, Solano, Emanuela, additional, Svenson, Karen L., additional, Thomas-Laemont, Patricia, additional, Threadgill, David W., additional, Ventura, Jacint, additional, Weinstock, George M., additional, Pomp, Daniel, additional, Churchill, Gary A., additional, and Pardo-Manuel de Villena, Fernando, additional

Published
2016
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176. Genetic analysis of complex traits in the emerging Collaborative Cross

Author

Collins, Francis S., Schwartz, David A., Aylor, David L., Steigerwalt, Jill, Ferris, Martin T., Chesler, Elissa J., Powell, Christine L., Frelinger, Jeff A., Bell, Timothy A., Branstetter, Lisa A., Hua, Kunjie, Baric, Ralph S., Frieman, Matt B., Valdar, William, Foulds-Mathes, Wendy, Verdugo, Ricardo A., Spence, Jason, McMillan, Leonard, Heise, Mark, Sarkar, Abhishek, Xie, Yuying, Miller, Darla R., Buus, Ryan J., Zhang, Qi, Didion, John D., Yang, Ivana V., Nehrenberg, Derrick L., Kelada, Samir N.P., Liu, Eric Yi, Wang, Wei, Gralinski, Lisa E., and Wang, Jeremy

Abstract

The Collaborative Cross (CC) is a mouse recombinant inbred strain panel that is being developed as a resource for mammalian systems genetics. Here we describe an experiment that uses partially inbred CC lines to evaluate the genetic properties and utility of this emerging resource. Genome-wide analysis of the incipient strains reveals high genetic diversity, balanced allele frequencies, and dense, evenly distributed recombination sites—all ideal qualities for a systems genetics resource. We map discrete, complex, and biomolecular traits and contrast two quantitative trait locus (QTL) mapping approaches. Analysis based on inferred haplotypes improves power, reduces false discovery, and provides information to identify and prioritize candidate genes that is unique to multifounder crosses like the CC. The number of expression QTLs discovered here exceeds all previous efforts at eQTL mapping in mice, and we map local eQTL at 1-Mb resolution. We demonstrate that the genetic diversity of the CC, which derives from random mixing of eight founder strains, results in high phenotypic diversity and enhances our ability to map causative loci underlying complex disease-related traits.

Published
2011
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178. Applying the ARRIVE Guidelines to an In Vivo Database.

Author

Karp, Natasha A, Karp, Natasha A, Meehan, Terry F, Morgan, Hugh, Mason, Jeremy C, Blake, Andrew, Kurbatova, Natalja, Smedley, Damian, Jacobsen, Julius, Mott, Richard F, Iyer, Vivek, Matthews, Peter, Melvin, David G, Wells, Sara, Flenniken, Ann M, Masuya, Hiroshi, Wakana, Shigeharu, White, Jacqueline K, Lloyd, KC Kent, Reynolds, Corey L, Paylor, Richard, West, David B, Svenson, Karen L, Chesler, Elissa J, de Angelis, Martin Hrabě, Tocchini-Valentini, Glauco P, Sorg, Tania, Herault, Yann, Parkinson, Helen, Mallon, Ann-Marie, Brown, Steve DM, Karp, Natasha A, Karp, Natasha A, Meehan, Terry F, Morgan, Hugh, Mason, Jeremy C, Blake, Andrew, Kurbatova, Natalja, Smedley, Damian, Jacobsen, Julius, Mott, Richard F, Iyer, Vivek, Matthews, Peter, Melvin, David G, Wells, Sara, Flenniken, Ann M, Masuya, Hiroshi, Wakana, Shigeharu, White, Jacqueline K, Lloyd, KC Kent, Reynolds, Corey L, Paylor, Richard, West, David B, Svenson, Karen L, Chesler, Elissa J, de Angelis, Martin Hrabě, Tocchini-Valentini, Glauco P, Sorg, Tania, Herault, Yann, Parkinson, Helen, Mallon, Ann-Marie, and Brown, Steve DM

Abstract

The Animal Research: Reporting of In Vivo Experiments (ARRIVE) guidelines were developed to address the lack of reproducibility in biomedical animal studies and improve the communication of research findings. While intended to guide the preparation of peer-reviewed manuscripts, the principles of transparent reporting are also fundamental for in vivo databases. Here, we describe the benefits and challenges of applying the guidelines for the International Mouse Phenotyping Consortium (IMPC), whose goal is to produce and phenotype 20,000 knockout mouse strains in a reproducible manner across ten research centres. In addition to ensuring the transparency and reproducibility of the IMPC, the solutions to the challenges of applying the ARRIVE guidelines in the context of IMPC will provide a resource to help guide similar initiatives in the future.

Published
2015

181. Analysis of sleep traits in knockout mice from the large-scale KOMP2 population using a non-invasive, high-throughput piezoelectric system

Author

Sethi, Mansi, primary, Joshi, Shreyas S, additional, Striz, Martin, additional, Cole, Neil, additional, Ryan, Jennifer, additional, Lhamon, Michael E, additional, Agarwal, Anuj, additional, Sukoff Rizzo, Stacey J, additional, Denegre, James M, additional, Braun, Robert E, additional, Fardo, David W, additional, Donohue, Kevin D, additional, Chesler, Elissa J, additional, Svenson, Karen L, additional, and O'Hara, Bruce F, additional

Published
2015
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185. R2d2 drives selfish sweeps in the house mouse

Author

Didion, John P, primary, Morgan, Andrew Parker, additional, Yadgary, Liran, additional, Bell, Timothy A, additional, McMullan, Rachel Clara, additional, Ortiz de Solorzano, Lydia, additional, Britton-Davidian, Janice, additional, Bult, Carol J, additional, Campbell, Karl J, additional, Castiglia, Riccardo, additional, Ching, Yung-Hao, additional, Chunco, Amanda J, additional, Crowley, James J, additional, Chesler, Elissa J, additional, French, John E, additional, Gabriel, Sofia I, additional, Gatti, Daniel M, additional, Garland, Theodore, additional, Giagia-Athanasopoulou, Eva B, additional, Giménez, Mabel D, additional, Grize, Sofia A, additional, Gündüz, İslam, additional, Holmes, Andrew, additional, Hauffe, Heidi C, additional, Herman, Jeremy S, additional, Holt, James M, additional, Hua, Kunji, additional, Jolley, Wesley J, additional, Lindholm, Anna K, additional, López-Fuster, María J, additional, Mitsainas, George, additional, Mathias, Maria, additional, McMillan, Leonard, additional, Ramalhinho, M Graça, additional, Rehermann, Barbara, additional, Rosshart, Stephan P, additional, Searle, Jeremy B, additional, Shiao, Meng-Shin, additional, Solano, Emanuela, additional, Svenson, Karen L, additional, Thomas-Laemont, Pat, additional, Threadgill, David W, additional, Ventura Queija, Jacint, additional, Weinstock, George M, additional, Pomp, Daniel, additional, Churchill, Gary A, additional, and Pardo-Manuel de Villena, Fernando, additional

Published
2015
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189. Aging Research Using Mouse Models

Author

Ackert‐Bicknell, Cheryl L., primary, Anderson, Laura C., additional, Sheehan, Susan, additional, Hill, Warren G., additional, Chang, Bo, additional, Churchill, Gary A., additional, Chesler, Elissa J., additional, Korstanje, Ron, additional, and Peters, Luanne L., additional

Published
2015
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190. Applying the ARRIVE Guidelines to an In Vivo Database

Author

Karp, Natasha A., primary, Meehan, Terry F., additional, Morgan, Hugh, additional, Mason, Jeremy C., additional, Blake, Andrew, additional, Kurbatova, Natalja, additional, Smedley, Damian, additional, Jacobsen, Julius, additional, Mott, Richard F., additional, Iyer, Vivek, additional, Matthews, Peter, additional, Melvin, David G., additional, Wells, Sara, additional, Flenniken, Ann M., additional, Masuya, Hiroshi, additional, Wakana, Shigeharu, additional, White, Jacqueline K., additional, Lloyd, K. C. Kent, additional, Reynolds, Corey L., additional, Paylor, Richard, additional, West, David B., additional, Svenson, Karen L., additional, Chesler, Elissa J., additional, de Angelis, Martin Hrabě, additional, Tocchini-Valentini, Glauco P., additional, Sorg, Tania, additional, Herault, Yann, additional, Parkinson, Helen, additional, Mallon, Ann-Marie, additional, and Brown, Steve D. M., additional

Published
2015
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191. A Multi-Megabase Copy Number Gain Causes Maternal Transmission Ratio Distortion on Mouse Chromosome 2

Author

Didion, John P., primary, Morgan, Andrew P., additional, Clayshulte, Amelia M.-F., additional, Mcmullan, Rachel C., additional, Yadgary, Liran, additional, Petkov, Petko M., additional, Bell, Timothy A., additional, Gatti, Daniel M., additional, Crowley, James J., additional, Hua, Kunjie, additional, Aylor, David L., additional, Bai, Ling, additional, Calaway, Mark, additional, Chesler, Elissa J., additional, French, John E., additional, Geiger, Thomas R., additional, Gooch, Terry J., additional, Garland, Theodore, additional, Harrill, Alison H., additional, Hunter, Kent, additional, McMillan, Leonard, additional, Holt, Matt, additional, Miller, Darla R., additional, O'Brien, Deborah A., additional, Paigen, Kenneth, additional, Pan, Wenqi, additional, Rowe, Lucy B., additional, Shaw, Ginger D., additional, Simecek, Petr, additional, Sullivan, Patrick F., additional, Svenson, Karen L, additional, Weinstock, George M., additional, Threadgill, David W., additional, Pomp, Daniel, additional, Churchill, Gary A., additional, and Pardo-Manuel de Villena, Fernando, additional

Published
2015
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192. KCNN Genes that Encode Small-Conductance Ca2+-Activated K+ Channels Influence Alcohol and Drug Addiction

Author

Padula, Audrey E, primary, Griffin, William C, additional, Lopez, Marcelo F, additional, Nimitvilai, Sudarat, additional, Cannady, Reginald, additional, McGuier, Natalie S, additional, Chesler, Elissa J, additional, Miles, Michael F, additional, Williams, Robert W, additional, Randall, Patrick K, additional, Woodward, John J, additional, Becker, Howard C, additional, and Mulholland, Patrick J, additional

Published
2015
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193. The Major Locus for Mouse Adenovirus Susceptibility Maps to Genes of the Hematopoietic Cell Surface-Expressed LY6 Family1

Author

Spindler, Katherine R., Welton, Amanda R., Lim, Efrem S., Duvvuru, Suman, Althaus, Irene W., Imperiale, Jennifer E., Daoud, Adam I., and Chesler, Elissa J.

Subjects
Male, Mice, Inbred BALB C, Mice, Inbred C3H, Mice, Inbred A, Quantitative Trait Loci, Chromosome Mapping, Hematopoietic Stem Cells, Article, Adenoviridae, Mice, Multigene Family, Animals, Antigens, Ly, Female, Genetic Predisposition to Disease, Alleles
Abstract

Susceptibility to mouse adenovirus type 1 is associated with the major quantitative trait locus Msq1. Msq1 was originally mapped to a 13-Mb region of mouse chromosome (Chr) 15 in crosses between SJL/J and BALB/cJ inbred mice. We have now narrowed Msq1 to a 0.75-Mb interval from 74.68 to 75.43 Mb, defined by two anonymous markers, rs8259436 and D15Spn14, using data from 1396 backcross mice. The critical interval includes 14 Ly6 or Ly6-related genes, including Ly6a (encoding Sca-1/TAP), Ly6e (Sca-2/Tsa1), Ly6g (Gr-1), and gpihbp1 (GPI-anchored high-density lipoprotein-binding protein 1), as well as the gene encoding an aldosterone synthase (Cyp11b2). The Ly6 family members are attractive candidates for virus susceptibility genes because their products are GPI-anchored membrane proteins expressed on lymphoid and myeloid cells, with proposed functions in cell adhesion and cell signaling. To determine interstrain variation in susceptibility and produce additional resources for cloning Msq1, we assayed the susceptibility phenotype of four previously untested inbred mouse strains. Susceptibility of strain 129S6/SvEvTac was subsequently localized to the Ly6 complex region, using polymorphic genetic markers on Chr 15 in a population of 271 (129S6/SvEvTac x BALB/cJ)F(1) x BALB/cJ backcross mice. We identified a major 129S6/SvEvTac susceptibility allele, Msq1(129S6), on Chr 15 in the same region as Msq1(SJL). The results indicate that a major host factor in mouse adenovirus type 1 susceptibility is likely to be a member of the Ly6 gene family.

Published
2010

194. Mouse Phenotype Database Integration Consortium: integration [corrected] of mouse phenome data resources

Author

Hancock, John M, Adams, Niels C, Aidinis, Vassilis, Blake, Andrew, Bogue, Molly, Brown, Steve D M, Chesler, Elissa J, Davidson, Duncan, Duran, Christopher, Eppig, Janan T, Gailus-Durner, Valérie, Gates, Hilary, Gkoutos, Georgios V, Greenaway, Simon, Hrabé de Angelis, Martin, Kollias, George, Leblanc, Sophie, Lee, Kirsty, Lengger, Christoph, Maier, Holger, Mallon, Ann-Marie, Masuya, Hiroshi, Melvin, David G, Müller, Werner, Parkinson, Helen, Proctor, Glenn, Reuveni, Eli, Schofield, Paul, Shukla, Aadya, Smith, Cynthia, Toyoda, Tetsuro, Vasseur, Laurent, Wakana, Shigeharu, Walling, Alison, White, Jacqui, Wood, Joe, and Zouberakis, Michalis

Subjects
Mice, Phenotype, Databases, Genetic, Animals, Mice, Inbred Strains, Genomics, Mice, Mutant Strains
Abstract

Understanding the functions encoded in the mouse genome will be central to an understanding of the genetic basis of human disease. To achieve this it will be essential to be able to characterize the phenotypic consequences of variation and alterations in individual genes. Data on the phenotypes of mouse strains are currently held in a number of different forms (detailed descriptions of mouse lines, first-line phenotyping data on novel mutations, data on the normal features of inbred lines) at many sites worldwide. For the most efficient use of these data sets, we have initiated a process to develop standards for the description of phenotypes (using ontologies) and file formats for the description of phenotyping protocols and phenotype data sets. This process is ongoing and needs to be supported by the wider mouse genetics and phenotyping communities to succeed. We invite interested parties to contact us as we develop this process further.

Published
2007

196. Mechanistic Differences in Neuropathic Pain Modalities Revealed by Correlating Behavior with Global Expression Profiling.

Author

Cobos, Enrique J., Nickerson, Chelsea A., Gao, Fuying, Chandran, Vijayendran, Bravo-Caparrós, Inmaculada, Gonzélez-Cano, Rafael, Riva, Priscilla, Andrews, Nick A., Latremoliere, Alban, Seehus, Corey R., Perazzoli, Gloria, Nieto, Francisco R., Joller, Nicole, Painter, Michio W., Chi Him Eddie Ma, Takao Omura, Chesler, Elissa J., Geschwind, Daniel H., Coppola, Giovanni, and Rangachari, Manu

Abstract

Chronic neuropathic pain is amajor morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia in a model of partial nerve injury and this temporal divergence was associated with major differences in global gene expression in innervating dorsal root ganglia. Transcripts whose expression change correlates with the onset of cold allodynia were nociceptor related, whereas those correlating with tactile hypersensitivity were immune cell centric. Ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity, whereas depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain incorporates reactive processes of sensory neurons and immune cells, each leading to distinct forms of hypersensitivity, potentially allowing drug development targeted to each pain type. [ABSTRACT FROM AUTHOR]

Published
2018
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197. Genetic networks controlling retinal injury

Author

Vazquez-Chona, Felix R., Khan, Amna N., Chan, Chun K., Moore, Anthony N., Dash, Pramod K., Hernandez, M. Rosario, Lu, Lu, Chesler, Elissa J., Manly, Kenneth F., Williams, Robert W., and Geisert, Eldon E.

Subjects
Wound Healing, Databases, Factual, Genetic Linkage, Gene Expression Profiling, Polymorphism, Single Nucleotide, Article, Retina, Rats, Mice, Inbred C57BL, Mice, Eye Injuries, Gene Expression Regulation, Meta-Analysis as Topic, Mice, Inbred DBA, Brain Injuries, Animals, Eye Proteins, Spinal Cord Injuries, Acute-Phase Proteins, Oligonucleotide Array Sequence Analysis, Transcription Factors
Abstract

The present study defines genomic loci underlying coordinate changes in gene expression following retinal injury.A group of acute phase genes expressed in diverse nervous system tissues was defined by combining microarray results from injury studies from rat retina, brain, and spinal cord. Genomic loci regulating the brain expression of acute phase genes were identified using a panel of BXD recombinant inbred (RI) mouse strains. Candidate upstream regulators within a locus were defined using single nucleotide polymorphism databases and promoter motif databases.The acute phase response of rat retina, brain, and spinal cord was dominated by transcription factors. Three genomic loci control transcript expression of acute phase genes in brains of BXD RI mouse strains. One locus was identified on chromosome 12 and was highly correlated with the expression of classic acute phase genes. Within the locus we identified the inhibitor of DNA binding 2 (Id2) as a candidate upstream regulator. Id2 was upregulated as an acute phase transcript in injury models of rat retina, brain, and spinal cord.We defined a group of transcriptional changes associated with the retinal acute injury response. Using genetic linkage analysis of natural transcript variation, we identified regulatory loci and candidate regulators that control transcript levels of acute phase genes.

Published
2005

198. Uncovering regulatory pathways that affect hematopoietic stem cell function using 'genetical genomics'

Author

Bystrykh, Leonid, Weersing, Ellen, Dontje, Bert, Sutton, Sue, Pletcher, Mathew T., Wiltshire, Tim, Su, Andrew I., Vellenga, Edo, Wang, Jintao, Manly, Kenneth F., Lu, Lu, Chesler, Elissa J., Alberts, Rudi, Jansen, Ritsert C., Williams, Robert W., Cooke, M., Pletcher, MT, de Haan, G, Su, AI, Wang, JT, Manly, KF, Chesler, EJ, Williams, O., and Bioinformatics

Subjects
Genetics, Candidate gene, IDENTIFICATION, Genome, Human, Molecular Sequence Data, Quantitative Trait Loci, Genomics, Quantitative trait locus, Biology, MOUSE, Hematopoietic Stem Cells, LESSONS, MICE, Gene mapping, Expression quantitative trait loci, Humans, Human genome, RNA, Messenger, Stem cell, Carrier Proteins, DISSECTION, Gene
Abstract

We combined large-scale mRNA expression analysis and gene mapping to identify genes and loci that control hematopoietic stem cell (HSC) function. We measured mRNA expression levels in purified HSCs isolated from a panel of densely genotyped recombinant inbred mouse strains. We mapped quantitative trait loci (QTLs) associated with variation in expression of thousands of transcripts. By comparing the physical transcript position with the location of the controlling QTL, we identified polymorphic cis-acting stem cell genes. We also identified multiple trans-acting control loci that modify expression of large numbers of genes. These groups of coregulated transcripts identify pathways that specify variation in stem cells. We illustrate this concept with the identification of candidate genes involved with HSC turnover. We compared expression QTLs in HSCs and brain from the same mice and identified both shared and tissue-specific QTLs. Our data are accessible through WebQTL, a web-based interface that allows custom genetic linkage analysis and identification of coregulated transcripts.

Published
2004

199. High-resolution sex-specific linkage maps of the mouse reveal polarized distribution of crossovers in male germline.

Author

Liu, Eric Yi, Liu, Eric Yi, Morgan, Andrew P, Chesler, Elissa J, Wang, Wei, Churchill, Gary A, Pardo-Manuel de Villena, Fernando, Liu, Eric Yi, Liu, Eric Yi, Morgan, Andrew P, Chesler, Elissa J, Wang, Wei, Churchill, Gary A, and Pardo-Manuel de Villena, Fernando

Abstract

Since the publication of the first comprehensive linkage map for the laboratory mouse, the architecture of recombination as a basic biological process has become amenable to investigation in mammalian model organisms. Here we take advantage of high-density genotyping and the unique pedigree structure of the incipient Collaborative Cross to investigate the roles of sex and genetic background in mammalian recombination. Our results confirm the observation that map length is longer when measured through female meiosis than through male meiosis, but we find that this difference is modified by genotype at loci on both the X chromosome and the autosomes. In addition, we report a striking concentration of crossovers in the distal ends of autosomes in male meiosis that is absent in female meiosis. The presence of this pattern in both single- and double-recombinant chromosomes, combined with the absence of a corresponding asymmetry in the distribution of double-strand breaks, indicates a regulated sequence of events specific to male meiosis that is anchored by chromosome ends. This pattern is consistent with the timing of chromosome pairing and evolutionary constraints on male recombination. Finally, we identify large regions of reduced crossover frequency that together encompass 5% of the genome. Many of these "cold regions" are enriched for segmental duplications, suggesting an inverse local correlation between recombination rate and mutation rate for large copy number variants.

Published
2014

200. Quantitative trait locus mapping methods for diversity outbred mice

Author

Gatti, Daniel M., Svenson, Karen L, Shabalin, Andrey, Wu, Long-Yang, Valder, William, Simecek, Petr, Goodwin, Neal, Cheng, Riyan, Pomp, Daniel, Palmer, Abraham, Chesler, Elissa J, Churchill, Gary A, Gatti, Daniel M., Svenson, Karen L, Shabalin, Andrey, Wu, Long-Yang, Valder, William, Simecek, Petr, Goodwin, Neal, Cheng, Riyan, Pomp, Daniel, Palmer, Abraham, Chesler, Elissa J, and Churchill, Gary A

Abstract

Genetic mapping studies in the mouse and other model organisms are used to search for genes underlying complex phenotypes. Traditional genetic mapping studies that employ single-generation crosses have poor mapping resolution and limit discovery to loci that are polymorphic between the two parental strains. Multiparent outbreeding populations address these shortcomings by increasing the density of recombination events and introducing allelic variants from multiple founder strains. However, multiparent crosses present new analytical challenges and require specialized software to take full advantage of these benefits. Each animal in an outbreeding population is genetically unique and must be genotyped using a high-density marker set; regression models for mapping must accommodate multiple founder alleles, and complex breeding designs give rise to polygenic covariance among related animals that must be accounted for in mapping analysis. The Diversity Outbred (DO) mice combine the genetic diversity of eight founder strains in a multigenerational breeding design that has been maintained for.16 generations. The large population size and randomized mating ensure the long-term genetic stability of this population. We present a complete analytical pipeline for genetic mapping in DO mice, including algorithms for probabilistic reconstruction of founder haplotypes from genotyping array intensity data, and mapping methods that accommodate multiple founder haplotypes and account for relatedness among animals. Power analysis suggests that studies with as few as 200 DO mice can detect loci with large effects, but loci that account for,5% of trait variance may require a sample size of up to 1000 animals. The methods described here are implemented in the freely available R package DOQTL.

Published
2014

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