The differentiation of the dermis in the laboratory mouse

1984 ◽  
Vol 169 (2) ◽  
pp. 149-164 ◽  
Author(s):  
Robert J. Van Exan ◽  
Margaret H. Hardy
Keyword(s):  
Author(s):  
Ricardo Wilches ◽  
William H Beluch ◽  
Ellen McConnell ◽  
Diethard Tautz ◽  
Yingguang Frank Chan

Abstract Most phenotypic traits in nature involve the collective action of many genes. Traits that evolve repeatedly are particularly useful for understanding how selection may act on changing trait values. In mice, large body size has evolved repeatedly on islands and under artificial selection in the laboratory. Identifying the loci and genes involved in this process may shed light on the evolution of complex, polygenic traits. Here, we have mapped the genetic basis of body size variation by making a genetic cross between mice from the Faroe Islands, which are among the largest and most distinctive natural populations of mice in the world, and a laboratory mouse strain selected for small body size, SM/J. Using this F2 intercross of 841 animals, we have identified 111 loci controlling various aspects of body size, weight and growth hormone levels. By comparing against other studies, including the use of a joint meta-analysis, we found that the loci involved in the evolution of large size in the Faroese mice were largely independent from those of a different island population or other laboratory strains. We hypothesize that colonization bottleneck, historical hybridization, or the redundancy between multiple loci have resulted in the Faroese mice achieving an outwardly similar phenotype through a distinct evolutionary path.


1988 ◽  
Vol 96 (4) ◽  
pp. 437-441 ◽  
Author(s):  
Umberto Filibeck ◽  
Simona Cabib ◽  
Claudio Castellano ◽  
Stefano Puglisi-Allegra

1997 ◽  
Vol 3 (S2) ◽  
pp. 317-318
Author(s):  
David A. Sanan ◽  
Dale L. Newland

Build-up of visible atherosclerotic plaque in the arteries is readily quantifiable. The mouse and the rabbit provide useful models for understanding the pathogenesis of atherosclerosis by investigating the effects of genetic and dietary perturbations.Although the wild type mouse does not develop atherosclerosis, atherosclerosis susceptibility genes have been identified in some laboratory mouse strains which do. Furthermore, transgenic technology and gene targeting have produced genetically modified mice that express various apolipoproteins, enzymes and cofactors involved in human lipoprotein metabolism. Gene “knockout” technology allows transgene expression without interference from homologous genes. One notable “knockout” mouse, deficient in apolipoprotein E, develops spontaneous atherosclerosis on a normal chow diet. Transgenic modulations of the atherosclerotic responses of these highly susceptible mice are more pronounced and easily measured. Small, cheap and fast breeding, mice are convenient animal models. But to make mice susceptible to atherosclerosis, their genetic background has to be so drastically altered that the resulting lipoprotein metabolism may not model the human metabolism accurately enough.


2009 ◽  
Vol 297 (3) ◽  
pp. R769-R774 ◽  
Author(s):  
Steven J. Swoap ◽  
Margaret J. Gutilla

The laboratory mouse is a facultative daily heterotherm in that it experiences bouts of torpor under caloric restriction. Mice are the most frequently studied laboratory mammal, and often, genetically modified mice are used to investigate many physiological functions related to weight loss and caloric intake. As such, research documenting the cardiovascular changes during fasting-induced torpor in mice is warranted. In the current study, C57BL/6 mice were implanted either with EKG/temperature telemeters or blood pressure telemeters. Upon fasting and exposure to an ambient temperature (Ta) of 19°C, mice entered torpor bouts as assessed by core body temperature (Tb). Core Tb fell from 36.6 ± 0.2°C to a minimum of 25.9 ± 0.9°C during the fast, with a concomitant fall in heart rate from 607 ± 12 beats per minute (bpm) to a minimum of 158 ± 20 bpm. Below a core Tb of 31°C, heart rate fell exponentially with Tb, and the Q10 was 2.61 ± 0.18. Further, mice implanted with blood pressure telemeters exhibited similar heart rate and activity profiles as those implanted with EKG/temperature telemeters, and the fall in heart rate and core Tb during entrance into torpor was paralleled by a fall in blood pressure. The minimum systolic, mean, and diastolic blood pressures of torpid mice were 62.3 ± 10.2, 51.9 ± 9.2, 41.0 ± 7.5 mmHg, respectively. Torpid mice had a significantly lower heart rate (25–35%) than when euthermic at mean arterial pressures from 75 to 100 mmHg, suggesting that total peripheral resistance is elevated during torpor. These data provide new and significant insight into the cardiovascular adjustments that occur in torpid mice.


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