Loss of H2A.Z Is Not Sufficient to Determine Transcriptional Activity of Snf2-Related CBP Activator Protein or p400 Complexes
2011

H2A.Z and Transcription Regulation by p400 and SRCAP Complexes

publication Evidence: moderate

Author Information

Author(s): Tamara A. Bowman, Madeline M. Wong, Linda K. Cox, Joseph J. Baldassare, John C. Chrivia

Primary Institution: Saint Louis University School of Medicine

Hypothesis

Do the p400 and SRCAP complexes play distinct roles in regulating transcription of the p21 promoter through deposition of H2A.Z into distinct populations of nucleosomes?

Conclusion

The deposition of H2A.Z by the p400 and SRCAP complexes is not sufficient to explain how they regulate transcription of the Sp1 and p21 promoters.

Supporting Evidence

  • Knockdown of SRCAP or p400 reduces deposition of H2A.Z by approximately 50%.
  • Loss of p400 expression activates transcription of the p21 promoter, while knockdown of SRCAP does not.
  • H2A.Z deposition is not targeted to specific nucleosomes but is broadly distributed.
  • Both SRCAP and p400 complexes have overlapping roles in H2A.Z deposition.

Takeaway

This study found that two protein complexes, p400 and SRCAP, help place a special protein called H2A.Z on DNA, but just putting H2A.Z on the DNA doesn't explain how they help turn genes on or off.

Methodology

The study used chromatin immunoprecipitation (ChIP) assays and quantitative real-time PCR to measure H2A.Z deposition and nucleosome density at the p21 and Sp1 promoters after knockdown of SRCAP or p400.

Limitations

The study does not explore the full range of potential mechanisms by which SRCAP and p400 may regulate transcription beyond H2A.Z deposition.

Digital Object Identifier (DOI)

10.1155/2011/715642

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