Genetic analysis of blood pressure in C3H/HeJ and SWR/J mice

1 The Jackson Laboratory, Bar Harbor, Maine 04609 2 Hypertension Section, Boston University School of Medicine, Boston, Massachusetts 02118 Hypertension is a complex phenotype induced by multiple environmental and genetic factors. Quantitative trait locus (QTL) analysis is a powerful method for iden...

Full description

Saved in:
Bibliographic Details
Published in:Physiological genomics 2004-04, Vol.17 (2), p.215-220
Main Authors: DiPetrillo, Keith, Tsaih, Shirng-Wern, Sheehan, Susan, Johns, Conrado, Kelmenson, Peter, Gavras, Haralambos, Churchill, Gary A, Paigen, Beverly
Format: Article
Language:English
Subjects:
Animals
Blood Pressure - genetics
Chromosome Mapping
Chromosomes, Mammalian
Crosses, Genetic
Female
Haplotypes
Heart Rate - genetics
Hypertension - genetics
Hypertension - physiopathology
Male
Mice
Mice, Inbred C3H
Mice, Inbred Strains
Quantitative Trait Loci
Sex Factors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:1 The Jackson Laboratory, Bar Harbor, Maine 04609 2 Hypertension Section, Boston University School of Medicine, Boston, Massachusetts 02118 Hypertension is a complex phenotype induced by multiple environmental and genetic factors. Quantitative trait locus (QTL) analysis is a powerful method for identifying genomic regions underlying complex diseases. We conducted a QTL analysis of blood pressure in mice using 217 F 2 progeny (males and females) from a cross between the normotensive C3H/HeJ and hypertensive SWR/J inbred strains. Our analysis identified significant QTL controlling blood pressure on chromosome 1 [Chr 1; Bpq8 ; peak 78 cM; 95% confidence interval 64–106 cM; logarithm of the odds ratio (LOD) 3.5; peak marker D1Mit105 ] and on Chr 16 ( Bpq9 ; peak 56 cM; 95% confidence interval 46–58 cM; LOD 3.6; peak marker D16Mit158 ). Bpq8 was previously identified in a cross between C57BL/6J and A/J mice, and we narrowed this QTL from 42 to 18 cM (95% confidence interval 68–86 cM) by combining the data from these crosses. By examining Bpq8 for regions where ancestral alleles were conserved among the high allele strains (C57BL/6J, SWR/J) and different from the low allele strains (A/J, C3H/HeJ), we identified a 2.3-cM region where the high allele strains shared a common haplotype. Bpq8 is concordant with known QTL in both rat and human, suggesting that the causal gene underlying Bpq8 may be conserved as a disease gene in human hypertension. quantitative trait loci; Bpq8 ; Bpq9
ISSN:1094-8341
1531-2267
DOI:10.1152/physiolgenomics.00212.2003