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Mapping exertional rhabdomyolysis ge...

Dranchak, Patricia K.

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Mapping exertional rhabdomyolysis genes in the horse.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Mapping exertional rhabdomyolysis genes in the horse./
Author:	Dranchak, Patricia K.
Description:	205 p.
Notes:	Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0671.
Contained By:	Dissertation Abstracts International67-02B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3207672
ISBN:	9780542559198

Mapping exertional rhabdomyolysis genes in the horse.
Dranchak, Patricia K.

Mapping exertional rhabdomyolysis genes in the horse. - 205 p.

Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0671.

Thesis (Ph.D.)--University of Minnesota, 2006.

The major goal of this thesis was to further define the molecular genetic basis of two different forms of exertional muscle disease in the horse. Recurrent exertional rhabdomyolysis (RER) in Thoroughbred racehorses is suggested to result from an alteration in the control of skeletal muscle contractility. Known RER and normal horses were mated to confirm the transmission of RER susceptibility to foals, as determined by increased sensitivity of intercostal muscle biopsies to halothane- and caffeine-induced contractures in vitro. The ratio of RER susceptible to normal foals was consistent with an autosomal dominant pattern of inheritance. Microsatellite markers at the RYR1, CACNA1S, ATP2A1, Ncx1, and Ncx3 candidate gene loci were developed and statistically excluded linkage to RER susceptibility in the breeding trial and three additional RER pedigrees. A whole genome scan with 398 microsatellite markers genotyped on these pedigrees excluded nearly 75% of the genome from containing the RER locus. Two regions of slightly suggestive linkage to RER were identified on ECA3 and 28.

ISBN: 9780542559198Subjects--Topical Terms:

1017730
Biology, Genetics.

Mapping exertional rhabdomyolysis genes in the horse.
LDR:03186nmm 2200313 4500 001 1828856
005 20071023113032.5
008 130610s2006 eng d
020 $a 9780542559198
035 $a (UMI)AAI3207672
035 $a AAI3207672
040 $a UMI $c UMI
100 1 $a Dranchak, Patricia K. $3 1917735
245 1 0 $a Mapping exertional rhabdomyolysis genes in the horse.
300 $a 205 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-02, Section: B, page: 0671.
500 $a Adviser: James R. Mickelson.
502 $a Thesis (Ph.D.)--University of Minnesota, 2006.
520 $a The major goal of this thesis was to further define the molecular genetic basis of two different forms of exertional muscle disease in the horse. Recurrent exertional rhabdomyolysis (RER) in Thoroughbred racehorses is suggested to result from an alteration in the control of skeletal muscle contractility. Known RER and normal horses were mated to confirm the transmission of RER susceptibility to foals, as determined by increased sensitivity of intercostal muscle biopsies to halothane- and caffeine-induced contractures in vitro. The ratio of RER susceptible to normal foals was consistent with an autosomal dominant pattern of inheritance. Microsatellite markers at the RYR1, CACNA1S, ATP2A1, Ncx1, and Ncx3 candidate gene loci were developed and statistically excluded linkage to RER susceptibility in the breeding trial and three additional RER pedigrees. A whole genome scan with 398 microsatellite markers genotyped on these pedigrees excluded nearly 75% of the genome from containing the RER locus. Two regions of slightly suggestive linkage to RER were identified on ECA3 and 28.
520 $a Polysaccharide storage myopathy (PSSM) in American Quarter Horses is characterized by increased insulin-regulated glucose uptake and excessive glycogen accumulation in skeletal muscle. Mutations in genes encoding the AMP activated protein kinase (AMPK) can cause similar alterations in glycogen metabolism in other species. Over 70% of the coding sequence, as well as radiation hybrid map assignments, for each of the seven subunits of the equine AMPK kinase gene family (PRKAA1, PRKAA2, PRKAB1, PRKAB2, PRKAG1, PRKAG2, and PRKAG3) were obtained. Association and linkage analysis with flanking microsatellites and intragenic SNP statistically excluded each of these genes from causing PSSM.
520 $a This thesis reports some of the first attempts to use the equine genome map to identify the chromosomal loci for heritable disease traits. Although major limitations in pedigree material, as well as microsatellite marker number and informativeness were encountered, new insights into the genetic bases for RER and PSSM were obtained. Future studies will likely utilize whole genome association and linkage disequilibrium approaches to attempt to identify the RER and PSSM genes.
590 $a School code: 0130.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Agriculture, Animal Pathology. $3 1021764
650 4 $a Biology, Veterinary Science. $3 1021733
690 $a 0369
690 $a 0476
690 $a 0778
710 2 0 $a University of Minnesota. $3 676231
773 0 $t Dissertation Abstracts International $g 67-02B.
790 1 0 $a Mickelson, James R., $e advisor
790 $a 0130
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3207672