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Genome Scan and Congenic Strains for Blood Pressure QTL Using Dahl Salt-Sensitive Rats
Author(s) -
Michael R. Garrett,
Howard Dene,
Roxanne Y. Walder,
Qianyun Zhang,
George T. Cicila,
Shahin Assadnia,
Alan Y. Deng,
John P. Rapp
Publication year - 1998
Publication title -
genome research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.556
H-Index - 297
eISSN - 1549-5469
pISSN - 1088-9051
DOI - 10.1101/gr.8.7.711
Subject(s) - quantitative trait locus , congenic , biology , genetics , allele , locus (genetics) , chromosome , genome scan , chromosome 9 , genetic linkage , population , blood pressure , chromosome 15 , gene , microsatellite , endocrinology , demography , sociology
An F 2 population ( n  = 151) derived from Dahl salt-sensitive (S) and Lewis rats was raised on a 8% NaCl diet for 9 weeks and analyzed for blood pressure quantitative trait loci (QTL) by use of a whole genome scan. Chromosomes 5 and 10 yielded lod scores for linkage to blood pressure that were significant; chromosomes 1, 2, 3, 8, 16, 17, and 18 gave lod scores suggestive for linkage. Chromosome 7 gave a significant signal for heart weight with a lesser effect on blood pressure. Congenic strains were constructed by introgressing Lewis low-blood-pressure QTL alleles for chromosomes 1, 5, 10, and 17 into the S genetic background. Congenic strains for chromosomes 1, 5, and 10 had significantly lower blood pressure than S, proving the existence of QTL on these chromosomes, but the chromosome 17 congenic strain failed to trap a contrasting QTL allele. The QTL allele increasing blood pressure originated from S rats for all QTL except those on chromosomes 2 and 7 in which the Lewis allele increased blood pressure. Interactions between each QTL and every other locus in the genome scan yielded significant interactions between chromosomes 10 and 4, and between chromosomes 2 and 3.

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