Document Detail


Sex-specific quantitative trait loci linked to autoresuscitation failure in SWR/J mice.
MedLine Citation:
PMID:  19654605     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Autoresuscitation (AR) is a highly conserved response among mammals, which allows survival from transient extreme hypoxia. During hypoxia, bradycardia, and hypoxic gasping develop after a brief period of hyperactivity. Normally, AR occurs if oxygen is restored during the gasping period where an initial heart rate increase is rapidly followed resumption or eupneic breathing. Humans and other mammals can survive multiple immediately repeated AR. A defective AR capacity has been implicated in Sudden Infant Death Syndrome. We had reported earlier that inbred strains of mice such as BALB/cJ could survive a characteristic number of immediately repeated AR trials, but that SWR/J mice failed to AR from a single hypoxic episode. We now report that strains closely related to SWR/J, FVB/N and SJL/J exhibit partial resuscitation defects relative to BALB/cJ or other mouse strains, establishing a genetic basis for variation in AR failure. The AR trial phenotype of BALB/cJ x SWR/J intercross F(1) and F(2) mice was consistent with BALB/cJ dominance and a discrete number of loci. Genome-wide mapping conducted with 60 intercross F(2) animals linked two loci to the number of AR trials survived, including one sex-specific locus with male expression, consistent with the observed 50% male bias for Sudden Infant Death Syndrome in humans. A locus carried on SWR/J chromosome 10 seems to be particularly important in AR failure and was confirmed in a partial consomic line. These results establish a genetic basis for AR failure phenotype in mice, with relevance to Sudden Infant Death Syndrome.
Authors:
B T Thach; J P Kenney-Hunt; T C Simon; J L Stratman; S B Thach; K A Harris; S Saunders; J M Cheverud
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2009-08-05
Journal Detail:
Title:  Heredity     Volume:  103     ISSN:  1365-2540     ISO Abbreviation:  Heredity (Edinb)     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-20     Completed Date:  2010-01-25     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0373007     Medline TA:  Heredity (Edinb)     Country:  England    
Other Details:
Languages:  eng     Pagination:  469-75     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA. Thach@kids.wustl.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / genetics,  physiopathology
Female
Humans
Male
Mice / genetics*,  physiology
Mice, Inbred Strains
Quantitative Trait Loci*
Respiratory Physiological Processes*
Sex Characteristics
Grant Support
ID/Acronym/Agency:
DK056063/DK/NIDDK NIH HHS; HD10993/HD/NICHD NIH HHS; HD33688/HD/NICHD NIH HHS; R01 DK056063-08/DK/NIDDK NIH HHS; R01 DK056063-08S1/DK/NIDDK NIH HHS; RR015116/RR/NCRR NIH HHS
Comments/Corrections
Comment In:
Heredity (Edinb). 2010 Oct;105(4):412   [PMID:  20332810 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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