Congenic strains confirm aerobic running capacity quantitative trait loci on rat chromosome 16 and identify possible intermediate phenotypes

2007 ◽  
Vol 29 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Justin A. Ways ◽  
Brian M. Smith ◽  
John C. Barbato ◽  
Ramona S. Ramdath ◽  
Krista M. Pettee ◽  
...  
Keyword(s):  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Strain Differences ◽  
Proximal Portion ◽  
Chromosome 16 ◽  
Rat Strains ◽  
High Performing ◽  
Intermediate Phenotypes ◽  
Trait Loci ◽  
Inbred Rat

We previously identified two inbred rat strains divergent for treadmill aerobic running capacity (ARC), the low-performing Copenhagen (COP) and the high-performing DA rats, and used an F2(COP×DA) population to identify ARC quantitative trait loci (QTLs) on rat chromosome 16 (RNO16) and the proximal portion of rat chromosome 3 (RNO3). Two congenic rat strains were bred to further investigate these ARC QTLs by introgressing RNO16 and the proximal portion of RNO3 from DA rats into the genetic background of COP rats and were named COP.DA(chr 16) and COP.DA(chr 3), respectively. COP.DA(chr 16) rats had significantly greater ARC compared with COP rats (696.7 ± 38.2 m vs. 571.9 ± 27.5 m, P = 0.03). COP.DA(chr 3) rats had increased, although not significant, ARC compared with COP rats (643.6 ± 40.9 m vs. 571.9 ± 27.5 m). COP.DA(chr 16) rats had significantly greater subcutaneous abdominal fat, as well as decreased fasting triglyceride levels, compared with COP rats ( P < 0.05), indicating that genes responsible for strain differences in fat metabolism are also located on RNO16. While this colocalization of QTLs may be coincidental, it is also possible that these differences in energy balance may be associated with the superior running performance of COP.DA(chr 16) consomic rats.

scholarly journals Tissue-Specific Actions of the Ept1, Ept2, Ept6, and Ept9 Genetic Determinants of Responsiveness to Estrogens in the Female Rat

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 3850-3859 ◽  
Author(s):  
Scott G. Kurz ◽  
Kimberly K. Hansen ◽  
Mac T. McLaughlin ◽  
Vijay Shivaswamy ◽  
Beverly S. Schaffer ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Quantitative Trait Loci ◽  
Pituitary Gland ◽  
Quantitative Trait ◽  
Mammary Cancer ◽  
Genetic Determinants ◽  
Rat Strains ◽  
Aci Rat ◽  
Trait Loci ◽  
Rat Strain

Ept1, Ept2, Ept6, and Ept9 are quantitative trait loci mapped in crosses between the ACI and Copenhagen (COP) rat strains as genetic determinants of responsiveness of the pituitary gland to estrogens. We have developed four congenic rat strains, each of which carries, on the genetic background of the ACI rat strain, alleles from the COP rat strain that span one of these quantitative trait loci. Relative to the female ACI rats, female ACI.COP-Ept1 rats exhibited reduced responsiveness to 17β-estradiol (E2) in the pituitary gland, as evidenced by quantification of pituitary mass and circulating prolactin, and in the mammary gland, as evidenced by reduced susceptibility to E2-induced mammary cancer. The ACI.COP-Ept2 rat strain exhibited reduced responsiveness to E2 in the pituitary gland but did not differ from the ACI strain in regard to susceptibility to E2-induced mammary cancer. Interestingly, female Ept2 congenic rats exhibited increased responsiveness to E2 in the thymus, as evidenced by enhanced thymic atrophy. The ACI.COP-Ept6 rat strain exhibited increased responsiveness to E2 in the pituitary gland, which was associated with a qualitative phenotype suggestive of enhanced pituitary vascularization. The ACI.COP-Ept9 rat strain exhibited reduced responsiveness to E2 in the anterior pituitary gland, relative to the ACI rat strain. Neither Ept6 nor Ept9 impacted responsiveness to E2 in the mammary gland or thymus. These data indicate that each of these Ept genetic determinants of estrogen action is unique in regard to the tissues in which it exerts its effects and/or the direction of its effect on estrogen responsiveness.

Interactions in hypoxic and hypercapnic breathing are genetically linked to mouse chromosomes 1 and 5

2004 ◽  
Vol 97 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Clarke G. Tankersley ◽  
Karl W. Broman
Keyword(s):  
Quantitative Trait Loci ◽  
Mouse Chromosome ◽  
Quantitative Trait ◽  
Odds Ratio ◽  
Genetic Model ◽  
Strain Differences ◽  
Interactive Effects ◽  
Chromosome 1 ◽  
Whole Body ◽  
Trait Loci

The genetic basis for differences in the regulation of breathing is certainly multigenic. The present paper builds on a well-established genetic model of differences in breathing using inbred mouse strains. We tested the interactive effects of hypoxia and hypercapnia in two strains of mice known for variation in hypercapnic ventilatory sensitivity (HCVS); i.e., high gain in C57BL/6J (B6) and low gain in C3H/HeJ (C3) mice. Strain differences in the magnitude and pattern of breathing were measured during normoxia [inspired O2 fraction (FiO2) = 0.21] and hypoxia (FiO2 = 0.10) with mild or severe hypercapnia (inspired CO2 fraction = 0.03 or 0.08) using whole body plethysmography. At each level of FiO2, the change in minute ventilation (V̇e) from 3 to 8% CO2 was computed, and the strain differences between B6 and C3 mice in HCVS were maintained. Inheritance patterns showed potentiation effects of hypoxia on HCVS (i.e., CO2 potentiation) unique to the B6C3F1/J offspring of B6 and C3 progenitors; i.e., the change in V̇e from 3 to 8% CO2 was significantly greater ( P < 0.01) with hypoxia relative to normoxia in F1 mice. Linkage analysis using intercross progeny (F2; n = 52) of B6 and C3 progenitors revealed two significant quantitative trait loci associated with variable HCVS phenotypes. After normalization for body weight, variation in V̇e responses during 8% CO2 in hypoxia was linked to mouse chromosome 1 (logarithm of the odds ratio = 4.4) in an interval between 68 and 89 cM (i.e., between D1Mit14 and D1Mit291). The second quantitative trait loci linked differences in CO2 potentiation to mouse chromosome 5 (logarithm of the odds ratio = 3.7) in a region between 7 and 29 cM (i.e., centered at D5Mit66). In conclusion, these results support the hypothesis that a minimum of two significant genes modulate the interactive effects of hypoxia and hypercapnia in this genetic model.

scholarly journals Chromosome-substituted rat strains provide insights into the genetics of placentation

2011 ◽  
Vol 43 (15) ◽  
pp. 930-941 ◽  
Author(s):  
Toshihiro Konno ◽  
Lea A. Rempel ◽  
M. A. Karim Rumi ◽  
Amanda R. Graham ◽  
Kazuo Asanoma ◽  
...  
Keyword(s):  
Quantitative Trait ◽  
Strain Differences ◽  
Transcript Level ◽  
Trophoblast Invasion ◽  
Brown Norway ◽  
Sprague Dawley ◽  
Rat Strains ◽  
Junctional Zone ◽  
Transcript Levels ◽  
Inbred Rat

The rat possesses a hemochorial form of placentation. Pronounced intrauterine trophoblast cell invasion and vascular remodeling characterize this type of placentation. Strain-specific patterns of placentation are evident in the rat. Some rat strains exhibit deep intrauterine trophoblast invasion and an expanded junctional zone [Holtzman Sprague-Dawley (HSD), Dahl salt sensitive (DSS)], whereas placentation sites of other rat strains are characterized by shallow invasion and a restricted junctional zone [Brown Norway (BN)]. In this report, we identified a quantitative trait that was used to distinguish strain-specific features of rat placentation. Junctional zone prolactin family 5, subfamily a, member 1 ( Prl5a1) transcript levels were significantly greater in BN rats than in HSD or DSS rats. Prl5a1 transcript levels were used as a quantitative trait to screen placentation sites from chromosome-substituted rat strains (BN chromosomes introgressed into the DSS inbred strain; DSS-BN panel). Litter size, placental weights, and fetal weights were not significantly different among the chromosome-substituted strains. Regulation of the junctional zone Prl5a1 transcript-level quantitative trait was multifactoral. Chromosome-substituted strains possessing BN chromosomes 14 or 17 introgressed into the DSS inbred rat strain displayed Prl5a1 transcript levels that were significantly different from the DSS pattern and more closely resembled the BN pattern. The in situ placental distribution of Prl5a1 mRNA and the structure of the junctional zone of DSS-BN17 rats mimicked that observed for the BN rat. Prl5a1 gene expression was also assessed in BN vs. HSD trophoblast stem cells and following reciprocal BN and HSD embryo transfer. Strain differences intrinsic to trophoblast and maternal environment were identified. In summary, we have identified chromosomes 14 and 17 as possessing regulatory information controlling a quantitative trait associated with rat placentation.

The mapping of quantitative trait loci underlying strain differences in locomotor activity between 129S6 and C57BL/6J mice

2003 ◽  
Vol 14 (10) ◽  
pp. 692-702 ◽  
Author(s):  
Michele A. Kelly ◽  
Malcolm J. Low ◽  
Tamara J. Phillips ◽  
Edward K. Wakeland ◽  
Masashi Yanagisawa
Keyword(s):  
Quantitative Trait Loci ◽  
Locomotor Activity ◽  
Quantitative Trait ◽  
Strain Differences ◽  
Trait Loci

scholarly journals Two Quantitative Trait Loci for Prepulse Inhibition of Startle Identified on Mouse Chromosome 16 Using Chromosome Substitution Strains

Genetics ◽  
2005 ◽  
Vol 171 (4) ◽  
pp. 1895-1904 ◽  
Author(s):  
Tracey L. Petryshen ◽  
Andrew Kirby ◽  
Ronald P. Hammer ◽  
Shaun Purcell ◽  
Sinead B. O'Leary ◽  
...  
Keyword(s):  
Quantitative Trait Loci ◽  
Mouse Chromosome ◽  
Prepulse Inhibition ◽  
Quantitative Trait ◽  
Chromosome Substitution ◽  
Chromosome 16 ◽  
Trait Loci ◽  
Chromosome Substitution Strains

Identification of cis-regulated genes in quantitative trait loci driving liver fibrosis

2012 ◽  
Vol 50 (08) ◽  
Author(s):  
R Hall ◽  
R Müllenbach ◽  
S Huss ◽  
R Alberts ◽  
K Schughart ◽  
...  
Keyword(s):  
Quantitative Trait Loci ◽  
Liver Fibrosis ◽  
Quantitative Trait ◽  
Trait Loci
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