Transcription profiling of mouse heart from cardiac-specific conditional knockout deletion of menage-a-trios-1 (MAT1)

ABSTRACT: The Cdk7/cyclin H/menage-a-trois 1 (MAT1) heterotrimer has proposed functions in transcription as the kinase component of basal transcription factor TFIIH and is activated in adult hearts by hypertrophic pathways. Using cardiac-specific Cre, we ablated MAT1 in myocardium. Despite reduced Cdk7 activity, MAT1-deficient hearts grew normally. However, fatal heart failure ensued at 6-8 weeks. By microarray profiling, quantitative RT-PCR, and Western blotting at 4 weeks, genes for energy metabolism were found to be suppressed selectively, including targets of peroxisome proliferator-activated receptor-gamma coactivator-1 (PGC-1). Cardiac metabolic defects were substantiated in isolated perfused hearts and isolated mitochondria. In culture, deleting MAT1 with Cre disrupted PGC-1 function: PGC-1α

ORGANISM(S): Mus musculus

SUBMITTER: Michael Schneider 

PROVIDER: E-GEOD-6662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress