Author: Ndao, Momar ; Diez, Eduardo ; Castellani, Lawrence W. ; Dubé, Marie-Pierre ; Fortin, Anny ; Vidal, Silvia M. ; Lafrenière, Ronald G. ; Paquette, Olivier ; Gagné, Mireille ; Miao, Qianqian ; Skamene, Emil ; Wiltshire, Sean A.

Epidemiological studies show that high HDL-cholesterol (HDLc) decreases the risk of cardiovascular disease. To map genes controlling lipid metabolism, particularly HDLc levels, we screened the plasma lipids of 36 AcB/BcA RC mouse strains subjected to either a normal or a high-fat/cholesterol diet. Strains BcA68 and AcB65 showed deviant HDLc plasma levels compared with the parental A/J and C57BL/6J strains; they were thus selected to generate informative F2 crosses. Linkage analyses in the AcB65 strain identified a locus on chromosome 4 ( Hdlq78) responsible for high post-high fat diet HDLc levels. This locus has been previously associated at genome-wide significance to two regions in the human genome. A second linkage analysis in strain BcA68 identified linkage in the vicinity of a gene cluster known to control HDLc levels. Sequence analysis of these candidates identified a de novo, loss-of-function mutation in the ApoA1 gene of BcA68 that prematurely truncates the ApoA1 protein. The possibility of dissecting the specific effects of this new ApoA1 deficiency in the context of isogenic controls makes the BcA68 mouse a valuable new tool.

01 Dec 2011·Nature NeuroscienceQ1 · MEDICINE

Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction

Q1 · MEDICINE

Article

Author: John K. Neubert ; Rosalie A. Bittong ; Jeffrey S. Mogil ; Robert R. Edwards ; William R. Lariviere ; Susana G. Sotocinal ; Inna Belfer ; J. Brad Mokris ; Jennifer Ritchie ; Roger B. Fillingim ; Anny Fortin ; Jan Czerminski ; Wendy F. Sternberg ; Claudia M. Campbell ; Jean Sebastien Austin ; James N. Campbell ; Kara Melmed ; Carey D. Balaban ; Margaret R. Wallace ; Robert E. Sorge ; Michael L. Lacroix-Fralish ; Shad B. Smith ; Ara Schorscher-Petcu ; Jacqueline N. Crawley

Quantitative trait locus mapping of chemical/inflammatory pain in the mouse identified the Avpr1a gene, which encodes the vasopressin-1A receptor (V1AR), as being responsible for strain-dependent pain sensitivity to formalin and capsaicin. A genetic association study in humans revealed the influence of a single nucleotide polymorphism (rs10877969) in AVPR1A on capsaicin pain levels, but only in male subjects reporting stress at the time of testing. The analgesic efficacy of the vasopressin analog desmopressin revealed a similar interaction between the drug and acute stress, as desmopressin inhibition of capsaicin pain was only observed in nonstressed subjects. Additional experiments in mice confirmed the male-specific interaction of V1AR and stress, leading to the conclusion that vasopressin activates endogenous analgesia mechanisms unless they have already been activated by stress. These findings represent, to the best of our knowledge, the first explicit demonstration of analgesic efficacy depending on the emotional state of the recipient, and illustrate the heuristic power of a bench-to-bedside-to-bench translational strategy.

03 Mar 2008·Genetic Susceptibility to Infectious Diseases

Mouse Models for Genetic Susceptibility to Infection in Humans

Author: Fortin, Anny ; Buschman, Ellen ; Skamene, Emil

AbstractOver the last several years, there has been a remarkable increase in the availability of new genomic strategies for analysis of complex traits in both human populations and mouse models. The advances in genome mapping, scanning, and analysis have been particularly valuable in the field of infectious diseases, leading to the cloning of a human gene for susceptibility to leprosy (Mira et al., 2003, 2004). In the mouse, the advent of genome scanning and new genetic strains has led to the identification of resistance=susceptibility loci for a large number of viral, bacterial, and eukaryotic pathogens. In the mammalian host, genetic control of resistance to infection (encompassing both innate and acquired immune phases) is regarded as a complex phenotype. In order to identify genes influencing host response to infection, the infectious process can be strategically divided into four stages: exposure to the pathogen, establishment of infection, progression of infection to disease, and clinical manifestation of the disease. Within these stages, the most important points of possible genetic control are likely to act during the innate and acquired phases of immunity.

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