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1 The Jackson Laboratory, Bar Harbor, ME, USA
2 Hypertension Section, Boston University, School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: bjp{at}jax.org.
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 F2 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 (Bpq8; peak 78cM; 95% confidence interval 64-106cM; LOD 3.5; peak marker D1Mit105) and on Chromosome 16 (Bpq9; peak 56cM; 95% confidence interval 46-58cM; 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 42cM to 18cM (95% confidence interval 68-86cM) 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.
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