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 ◽  
...  
Genetics ◽  
2004 ◽  
Vol 169 (2) ◽  
pp. 855-862 ◽  
Author(s):  
Jonathan B. Singer ◽  
Annie E. Hill ◽  
Joseph H. Nadeau ◽  
Eric S. Lander

2007 ◽  
Vol 29 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Justin A. Ways ◽  
Brian M. Smith ◽  
John C. Barbato ◽  
Ramona S. Ramdath ◽  
Krista M. Pettee ◽  
...  

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.


2007 ◽  
Vol 15 (6) ◽  
pp. 922-927 ◽  
Author(s):  
Hongrun Yu ◽  
David J. Baylink ◽  
Godfred L. Masinde ◽  
Runzhi Li ◽  
Bay Nguyen ◽  
...  

1998 ◽  
Vol 47 (4) ◽  
pp. 326-331 ◽  
Author(s):  
A. Puel ◽  
Jean-Claude Mevel ◽  
Yolande Bouthillier ◽  
Claude Decreusefond ◽  
Wolf H. Fridman ◽  
...  

2003 ◽  
Vol 165 (3) ◽  
pp. 270-279 ◽  
Author(s):  
Abraham A. Palmer ◽  
Laura L. Breen ◽  
Pamela Flodman ◽  
Lisa H. Conti ◽  
Anne M. Spence ◽  
...  

2004 ◽  
Vol 97 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Clarke G. Tankersley ◽  
Karl W. Broman

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.


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