Abstract
Identification of a Cardiac Disease Modifier Gene Using Forward Genetics in the Mouse
Highlights
This team reported strain background–dependent differences in heart failure endpoints, including left ventricular contraction and survival, for the calsequestrin (Casq1 or CSQ) transgenic model of dilated cardiomyopathy [3,4]
Congenic mice containing the AKR Hrtfm2 region isolated in a DBA background exhibited both increased Tnni3k expression and accelerated death of CSQ transgenics
Tnni3k encodes a cardiac-restricted kinase that belongs to the MAPKKK family, with homology to integrin-linked kinase (Ilk), Raf1, and Tak1 (MGI: Map3k7) [6]
Summary
This team reported strain background–dependent differences in heart failure endpoints, including left ventricular contraction and survival, for the calsequestrin (Casq1 or CSQ) transgenic model of dilated cardiomyopathy [3,4]. Heart failure and death were accelerated when the CSQ transgene was crossed into the inbred C57BL6/J (B6) compared to the DBA/2J (DBA) strain background. Crosses between DBA/2J CSQ transgenic and AKR/J (AKR) mice identified a similar disease-accelerating locus mapping to the same chromosomal region, and haplotype analysis narrowed the candidate interval to 2 Mb, encompassing seven known genes [5].
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