Abstract

A zinc finger protein GATA4 is one of the hypertrophy-responsive transcription factors and forms a complex with an intrinsic histone acetyltransferase, p300. Disruption of this complex results in the inhibition of cardiomyocyte hypertrophy and heart failure in vivo. By tandem affinity purification and mass spectrometric analyses, we identified cyclin-dependent kinase-9 (Cdk9) as a novel GATA4-binding partner. Cdk9 also formed a complex with p300 as well as GATA4 and cyclin T1. We showed that p300 was required for the interaction of GATA4 with Cdk9 and for the kinase activity of Cdk9. Conversely, Cdk9 kinase activity was required for the p300-induced transcriptional activities, DNA binding, and acetylation of GATA4. Furthermore, the kinase activity of Cdk9 was required for the phosphorylation of p300 as well as for cardiomyocyte hypertrophy. These findings demonstrate that Cdk9 forms a functional complex with the p300/GATA4 and is required for p300/GATA4- transcriptional pathway during cardiomyocyte hypertrophy.

Highlights

  • Ger protein, GATA4 [3, 4]

  • The kinase activity of cyclin-dependent kinase 9 (Cdk9) was required for the phosphorylation of p300 as well as for cardiomyocyte hypertrophy. These findings demonstrate that Cdk9 forms a functional complex with the p300/GATA4 and is required for p300/GATA4- transcriptional pathway during cardiomyocyte hypertrophy

  • We examined the binding of cyclin T1, another component of pTEF-b, with p300 and GATA4 as well as Cdk9

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Summary

Introduction

Ger protein, GATA4 [3, 4]. GATA4 functionally and physically interacts with other transcription factors, including NFAT-3, GATA6, MEF-2, STAT, and SRF [5,6,7,8,9]. Cdk9 kinase activity was required for the p300-induced transcriptional activities, DNA binding, and acetylation of GATA4. Nuclear extracts from these cells were subjected to immunoprecipitation with anti-Cdk9, or IgG as a control, followed by Western blotting with anti-GATA4, antiGATA6, or anti-Cdk9 antibody.

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