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Mitochondrial genomic polymorphisms in rat genetic models of hypertension
Author(s) -
Kumarasamy Sivarajan,
Gopalakrishnan Kathirvel,
Thangavel Jayakumar,
Shafton Asher,
Nixon Jeremy,
Farms Phyllis,
Joe Bina
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.792.4
Subject(s) - nonsynonymous substitution , mitochondrial dna , biology , genome , gene , genetics , genetic variation , nuclear gene , spontaneously hypertensive rat , phenotype , mitochondrion , blood pressure , endocrinology
Hypertension is a complex trait that has been extensively studied for genetic contributions of the nuclear genome. However, recent studies indicate that naturally occurring variation in the mitochondrial genome contribute to several complex traits. We examined whether there are variations between the mitochondrial genomes of genetic models including the Dahl salt‐sensitive (S) rat, the Dahl salt‐resistant (R) rat, the spontaneously hypertensive rat (SHR) and the Albino Surgery (AS) rat. The results provide evidence to suggest that variations in the mitochondrial genome do not account for observed differences in blood pressure between the S rat and the R rat. However, a total of 105, 99 and 18 variations in mtDNA were observed between the three comparisons‐S and SHR, S and AS and SHR and AS, respectively. Among the 13 protein coding genes of the mtDNA, 8 genes possessed nonsynonymous variations between S, SHR and AS. While the lack of any sequence variants between the mitochondrial genomes of S and R rats provides conclusive evidence that divergence in blood pressure between these two inbred strains is exclusively programmed through their nuclear genomes, the variations detected among the various hypertensive strains provides the basis to construct conplastic strains and further evaluate the effects of these variants on hypertension and associated phenotypes.