Journal
GENOME BIOLOGY
Volume 18, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s13059-017-1221-3
Keywords
H3.3; Histone variants; H2A.Z; Linker histone H1; DNA methylation; Chromatin
Funding
- Temasek LifeSciences Laboratory
- Gregor Mendel Institute
- FWF grant [P 28320-B21]
- EMBO fellowship [ALTF 1129-2013]
- Dissertation Year Fellowship from UCLA
- NIH [GM60398]
- Japan Society for the Promotion of Science (Overseas Research Fellowship) [601]
- Japanese Ministry of Education, Culture, Sports, Science and Technology [19207002, 19060014]
- Grants-in-Aid for Scientific Research [19060014, 19207002, 26221105] Funding Source: KAKEN
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Background: Gene bodies of vertebrates and flowering plants are occupied by the histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. DNA methylation and H3.3 enrichment profiles over gene bodies are correlated and both have a similar dependence on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. Results: We engineered an H3.3 knockdown in Arabidopsis thaliana and observed transcription reduction that predominantly affects genes responsive to environmental cues. When H3.3 levels are reduced, gene bodies show a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome-wide distributions of several histone H3 marks, H2A. Z, and linker histone H1. We report that in the absence of H3.3, H1 distribution increases in gene bodies in a transcription-dependent manner. Conclusions: We propose that H3.3 prevents recruitment of H1, inhibiting H1' s promotion of chromatin folding that restricts access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in conjunction with transcriptional activity.
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