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Molecular and Cellular Biology, September 2001, p. 6270-6279, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6270-6279.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

H2A.Z Is Required for Global Chromatin Integrity and for Recruitment of RNA Polymerase II under Specific Conditions

Maryse Adam,1 François Robert,2 Marc Larochelle,1 and Luc Gaudreau1,*

Département de Biologie, Université de Sherbrooke, Sherbrooke, Québec J1K 2R1, Canada,1 and Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 021422

Received 23 March 2001/Returned for modification 25 April 2001/Accepted 14 June 2001

Evolutionarily conserved variant histone H2A.Z has been recently shown to regulate gene transcription in Saccharomyces cerevisiae. Here we show that loss of H2A.Z in this organism negatively affects the induction of GAL genes. Importantly, fusion of the H2A.Z C-terminal region to S phase H2A without its corresponding C-terminal region can mediate the variant histone's specialized function in GAL1-10 gene induction, and it restores the slow-growth phenotype of cells with a deletion of HTZ1. Furthermore, we show that the C-terminal region of H2A.Z can interact with some components of the transcriptional apparatus. In cells lacking H2A.Z, recruitment of RNA polymerase II and TATA-binding protein to the GAL1-10 promoters is significantly diminished under inducing conditions. Unexpectedly, we also find that H2A.Z is required to globally maintain chromatin integrity under GAL gene-inducing conditions. We hypothesize that H2A.Z can positively regulate gene transcription, at least in part, by modulating interactions with RNA polymerase II-associated factors at certain genes under specific cell growth conditions.

* Corresponding author. Mailing address: Département de Biologie, Université de Sherbrooke, Sherbrooke, Québec J1K 2R1, Canada. Phone: (819) 821-8000, ext. 2081. Fax: (819) 821-8049. E-mail: luc.gaudreau{at}courrier.usherb.ca.

Molecular and Cellular Biology, September 2001, p. 6270-6279, Vol. 21, No. 18
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.18.6270-6279.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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