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

Loss of histone H3K36 methylation results in arrhythmic frq transcription and a failure of the circadian clock.

• Deletion of the histone methyltransferase SET-2 or H3K36R mutation leads to arrhythmic frq transcription and loss of rhythmicity.
• Histone acetylation at the frq locus increases in the set-2 knockout mutant.
• Mutations in H3K36 methylation readers, such as histone deacetylase RPD-3 or EAF-3, also result in hyperacetylation and WC-independent frq expression.
• A mutant strain with three amino acid substitutions in histone H3 mimicking a hyperacetylation state exhibits a defective clock phenotype similar to the rpd-3 knockout mutant.
• H3K36 methylation appears to be essential for maintaining an appropriate chromatin structure necessary for circadian frq transcription.

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