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Plant Cell. 2017 Apr;29(4):791-807. doi: 10.1105/tpc.16.00573. Epub 2017 Mar 3.

Dual Role of the Histone Variant H2A.Z in Transcriptional Regulation of Stress-Response Genes.

Author information

1
Department of Biotechnology, Adam Mickiewicz University, 61-614 Poznan, Poland.
2
Department of Bioinformatics, Adam Mickiewicz University, 61-614 Poznan, Poland.
3
Department of Computational Biology, Adam Mickiewicz University, 61-614 Poznan, Poland.
4
Department of Biotechnology, Adam Mickiewicz University, 61-614 Poznan, Poland pzio@amu.edu.pl.

Abstract

The influence of the histone variant H2A.Z on transcription remains a long-standing conundrum. Here, by analyzing the actin-related protein6 mutant, which is impaired in H2A.Z deposition, and by H2A.Z profiling in stress conditions, we investigated the impact of this histone variant on gene expression in Arabidopsis thaliana We demonstrate that the arp6 mutant exhibits anomalies in response to osmotic stress. Indeed, stress-responsive genes are overrepresented among those hyperactive in arp6. In wild-type plants, these genes exhibit high levels of H2A.Z in the gene body. Furthermore, we observed that in drought-responsive genes, levels of H2A.Z in the gene body correlate with transcript levels. H2A.Z occupancy, but not distribution, changes in parallel with transcriptional changes. In particular, we observed H2A.Z loss upon transcriptional activation and H2A.Z gain upon repression. These data suggest that H2A.Z has a repressive role in transcription and counteracts unwanted expression in noninductive conditions. However, reduced activity of some genes in arp6 is associated with distinct behavior of H2A.Z at their +1 nucleosome, which exemplifies the requirement of this histone for transcription. Our data support a model where H2A.Z in gene bodies has a strong repressive effect on transcription, whereas in +1 nucleosomes, it is important for maintaining the activity of some genes.

PMID:
28258158
PMCID:
PMC5435421
DOI:
10.1105/tpc.16.00573
[Indexed for MEDLINE]
Free PMC Article

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