@article{mathes_aylor_miller_churchill_chesler_villena_threadgill_pomp_2011, title={Architecture of energy balance traits in emerging lines of the Collaborative Cross}, volume={300}, ISSN={["1522-1555"]}, DOI={10.1152/ajpendo.00707.2010}, abstractNote={The potential utility of the Collaborative Cross (CC) mouse resource was evaluated to better understand complex traits related to energy balance. A primary focus was to examine if genetic diversity in emerging CC lines (pre-CC) would translate into equivalent phenotypic diversity. Second, we mapped quantitative trait loci (QTL) for 15 metabolism- and exercise-related phenotypes in this population. We evaluated metabolic and voluntary exercise traits in 176 pre-CC lines, revealing phenotypic variation often exceeding that seen across the eight founder strains from which the pre-CC was derived. Many phenotypic correlations existing within the founder strains were no longer significant in the pre-CC population, potentially representing reduced linkage disequilibrium (LD) of regions harboring multiple genes with effects on energy balance or disruption of genetic structure of extant inbred strains with substantial shared ancestry. QTL mapping revealed five significant and eight suggestive QTL for body weight (Chr 4, 7.54 Mb; CI 3.32–10.34 Mb; Bwq14), body composition, wheel running (Chr 16, 33.2 Mb; CI 32.5–38.3 Mb), body weight change in response to exercise (1: Chr 6, 77.7Mb; CI 72.2–83.4 Mb and 2: Chr 6, 42.8 Mb; CI 39.4–48.1 Mb), and food intake during exercise (Chr 12, 85.1 Mb; CI 82.9–89.0 Mb). Some QTL overlapped with previously mapped QTL for similar traits, whereas other QTL appear to represent novel loci. These results suggest that the CC will be a powerful, high-precision tool for examining the genetic architecture of complex traits such as those involved in regulation of energy balance.}, number={6}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM}, author={Mathes, Wendy Foulds and Aylor, David L. and Miller, Darla R. and Churchill, Gary A. and Chesler, Elissa J. and Villena, Fernando Pardo-Manuel and Threadgill, David W. and Pomp, Daniel}, year={2011}, month={Jun}, pages={E1124–E1134} }
 @article{la merrill_kuruvilla_pomp_birnbaum_threadgill_2009, title={Dietary Fat Alters Body Composition, Mammary Development, and Cytochrome P450 Induction after Maternal TCDD Exposure in DBA/2J Mice with Low-Responsive Aryl Hydrocarbon Receptors}, volume={117}, ISSN={["1552-9924"]}, DOI={10.1289/ehp.0800530}, abstractNote={Background Increased fat intake is associated with obesity and may make obese individuals uniquely susceptible to the effects of lipophilic aryl hydrocarbon receptor (AHR) ligands. Objectives We investigated the consequences of high-fat diet (HFD) and AHR ligands on body composition, mammary development, and hepatic P450 expression. Methods Pregnant C57BL/6J (B6) and DBA/2J (D2) dams, respectively expressing high- or low-responsive AHR, were dosed at mid-gestation with TCDD. At parturition, mice were placed on an HFD or a low-fat diet (LFD). Body fat of progeny was measured before dosing with 7,12-dimethylbenz[a]anthracene (DMBA). Fasting blood glucose was measured, and liver and mammary glands were analyzed. Results Maternal TCDD exposure resulted in reduced litter size in D2 mice and, on HFD, reduced postpartum survival in B6 mice. In D2 mice, HFD increased body mass and fat in off-spring, induced precocious mammary gland development, and increased AHR expression compared with mice given an LFD. Maternal TCDD exposure increased hepatic Cyp1a1 and Cyp1b1 expression in offspring on both diets, but DMBA depressed Cyp1b1 expression only in mice fed an HFD. In D2 progeny, TCDD exposure decreased mammary terminal end bud size, and DMBA exposure decreased the number of terminal end buds. Only in D2 progeny fed HFD did perinatal TCDD increase blood glucose and the size of mammary fat pads, while decreasing both branch elongation and the number of terminal end buds. Conclusions We conclude that despite having a low-responsive AHR, D2 progeny fed a diet similar to that consumed by most people are susceptible to TCDD and DMBA exposure effects blood glucose levels, mammary differentiation, and hepatic Cyp1 expression.}, number={9}, journal={ENVIRONMENTAL HEALTH PERSPECTIVES}, author={La Merrill, Michele and Kuruvilla, Bittu S. and Pomp, Daniel and Birnbaum, Linda S. and Threadgill, David W.}, year={2009}, month={Sep}, pages={1414–1419} }
 @article{pomp_eisen_1991, title={GENETIC-VARIATION IN REPRODUCTIVE RESPONSES TO A HIGH-ENERGY DIET IN MICE}, volume={69}, ISSN={["0021-8812"]}, DOI={10.2527/1991.6951875x}, abstractNote={Effects of a high-energy diet on reproduction were studied in 300 mice from lines selected for litter size and(or) 6-wk BW (L+, increased litter size; W+, increased body weight; L+W-, increased litter size and decreased body weight; L-W+, decreased litter size and increased body weight; and K, randomly selected control). Mice received a high-energy diet (HED; 3.8 kcal/g of ME) or a standard diet (STD; 3.3 kcal/g of ME) from 8 to 11 wk of age and were then mated and evaluated for ovulation rate and embryo survival through 17 d of gestation. The HED increased ovulation rate in all lines (P less than .05). The line x diet interaction was significant, with increased ovulation rate due to HED ranging from 9.9% in W+ to 24.2% in L-W+. Within-line regression coefficients of ovulation rate on ME intake (kilocalories from 10 to 11 wk) varied from .08 +/- .04 (P less than .05) in L+W- to .177 +/- .05 (P less than .01) in L+. In contrast, nonsignificant increases were observed in litter size (live fetuses at 17 d of gestation) due to HED. Effects of HED on embryo survival rate were significantly negative in L+ and L+W-; the decrease in L+ was a result of preimplantation losses, and the decrease in L+W- was due to postimplantation losses. The line x diet interaction was significant for postimplantation embryo survival. The results indicate significant genetic variation in reproductive responses to a high-energy diet in mice.}, number={5}, journal={JOURNAL OF ANIMAL SCIENCE}, author={POMP, D and EISEN, EJ}, year={1991}, month={May}, pages={1875–1884} }
 @article{pomp_eisen_1991, title={VARIATION AMONG DONOR FEMALES IN MAMMALIAN PREIMPLANTATION EMBRYO RESEARCH}, volume={35}, ISSN={["0093-691X"]}, DOI={10.1016/0093-691X(91)90367-M}, abstractNote={Data from two investigations involving preimplantation mouse embryo survival rates were analyzed by statistical methods which considered (Analysis I) or ignored (Analysis II) variation among-donor females. The first investigation studied in vitro development of zygotes in two culture media. Embryos from each donor female were randomly allocated to treatments. Analysis I utilized donor female as a block, removing among-donor female variation from the mean-square error. Analysis II ignored this variation, as if embryos from all donor females were pooled prior to random allocation to treatment. Media effects were large in both cases, and interpretation of results did not differ among analyses for an outbred stock or for an outbred × inbred cross. However, level of significance was consistently more extreme in Analysis II than in Analysis I. The second investigation studied genotypic responses in development of eight-cell embryos following cryopreservation. Survival rate was measured per donor female within genotype. Analysis I utilized donor females nested within genotype as the error term. Analysis II again utilized categorical pooling of data, ignoring donor females. In several cases, genotype differences and interaction effects were significant in Analysis II but not in Analysis I. Interpretation of results was dependent upon type of analysis. Consideration of among-donor female variation consistently yielded conservative tests of hypotheses relative to analyses which ignored this source of variation. Failure to consider among-donor female variation may lead to improper hypothesis testing, thus increasing the risk of false rejection of null hypotheses (Type-I error).}, number={6}, journal={THERIOGENOLOGY}, author={POMP, D and EISEN, EJ}, year={1991}, month={Jun}, pages={1209–1224} }
 @article{pomp_eisen_1990, title={GENETIC-CONTROL OF SURVIVAL OF FROZEN MOUSE EMBRYOS}, volume={42}, ISSN={["1529-7268"]}, DOI={10.1095/biolreprod42.5.775}, abstractNote={Lines of mice selected for increased litter size (L+), increased body weight (W+), or randomly (K) were used to study genetic variation in embryo cryosurvival in response to standard cryopreservation protocols. A total of 60528-cell embryos from 400 females were used in two studies. In Study 1, embryos from L+, W+, and K were frozen by slow-cool and ultrarapid (direct-plunge) methods to evaluate effects of selection on cryosurvival and genotype X freezing method interaction. Post-thaw survival (PTS) was measured as percentage of recovered embryos developing in vitro to blastocyst per donor female. Nonfrozen control embryos developed similarly for each line. Within slow-cool freezing, lines differed (W+ greater than K, W+ = L+, L+ = K; p less than 0.05); no differences were observed within the ultrarapid freezing. However, line X method interaction effects on PTS were not significant. In Study 2, reciprocal crosses were made between L+ and K and between W+ and K. Hybrid and pure line embryos were frozen by slow-cooling. Control embryos developed similarly for all genotypes. Selection lines did not differ for overall PTS. However, hybrid embryos from L+ dams were superior to those from K dams (84 vs. 61%; p less than .001). No overall embryo heterosis was observed. Differences were not significant among embryo genotypes or treatments for cell number or in vivo survival. These results demonstrate significant correlated responses in embryo post-thaw cryosurvival due to selection, and implicate both maternal and embryonic genomes as controlling mouse embryo cryosurvival.}, number={5-6}, journal={BIOLOGY OF REPRODUCTION}, author={POMP, D and EISEN, EJ}, year={1990}, pages={775–786} }
 @article{pomp_critser_1988, title={Cryopreservation of mammalian embryos}, volume={1}, number={1}, journal={ISI Atlas of Science}, author={Pomp, D. and Critser, J. K.}, year={1988}, pages={40} }