Suppression of WHITE COLLAR-independent frequency Transcription by Histone H3 Lysine 36 Methyltransferase SET-2 Is Necessary for Clock Function in Neurospora

The circadian system in Neurospora is based on the transcriptional/translational feedback loops and rhythmic frequency (frq) transcription requires the WHITE COLLAR (WC) complex. Our previous paper has shown that frq could be transcribed in a WC-independent pathway in a strain lacking the histone H3...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of biological chemistry 2016-05, Vol.291 (21), p.11055-11063
Main Authors: Sun, Guangyan, Zhou, Zhipeng, Liu, Xiao, Gai, Kexin, Liu, Qingqing, Cha, Joonseok, Kaleri, Farah Naz, Wang, Ying, He, Qun
Format: Article
Language:English
Subjects:
Circadian Clocks - genetics
circadian rhythm
clock gene
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Fungal Proteins - genetics
Fungal Proteins - metabolism
Gene Expression Regulation, Fungal
Gene Knockout Techniques
Gene Regulation
gene transcription
Genes, Fungal
Histone Deacetylases - genetics
Histone Deacetylases - metabolism
histone modification
Histone-Lysine N-Methyltransferase - deficiency
Histone-Lysine N-Methyltransferase - genetics
Histone-Lysine N-Methyltransferase - metabolism
Mutagenesis, Site-Directed
Mutant Proteins - genetics
Mutant Proteins - metabolism
Neurospora
Neurospora crassa - genetics
Neurospora crassa - metabolism
Recombinant Proteins - genetics
Recombinant Proteins - metabolism
SET-2 pathway
Transcription Factors - genetics
Transcription Factors - metabolism
WC-independent frq
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The circadian system in Neurospora is based on the transcriptional/translational feedback loops and rhythmic frequency (frq) transcription requires the WHITE COLLAR (WC) complex. Our previous paper has shown that frq could be transcribed in a WC-independent pathway in a strain lacking the histone H3K36 methyltransferase, SET-2 (su(var)3–9-enhancer-of-zeste-trithorax-2) (1), but the mechanism was unclear. Here we disclose that loss of histone H3K36 methylation, due to either deletion of SET-2 or H3K36R mutation, results in arrhythmic frq transcription and loss of overt rhythmicity. Histone acetylation at frq locus increases in set-2KO mutant. Consistent with these results, loss of H3K36 methylation readers, histone deacetylase RPD-3 (reduced potassium dependence 3) or EAF-3 (essential SAS-related acetyltransferase-associated factor 3), also leads to hyperacetylation of histone at frq locus and WC-independent frq expression, suggesting that proper chromatin modification at frq locus is required for circadian clock operation. Furthermore, a mutant strain with three amino acid substitutions (histone H3 lysine 9, 14, and 18 to glutamine) was generated to mimic the strain with hyperacetylation state of histone H3. H3K9QK14QK18Q mutant exhibits the same defective clock phenotype as rpd-3KO mutant. Our results support a scenario in which H3K36 methylation is required to establish a permissive chromatin state for circadian frq transcription by maintaining proper acetylation status at frq locus.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M115.711333