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Circadian-regulated gene expression is predominantly controlled by a transcriptional negative feedback loop, and it is evident that chromatin modifications and chromatin remodeling are integral to this process in eukaryotes. We previously determined that multiple ATP–dependent chromatin-remodeling enzymes function at  frequency  ( frq ). In this report, we demonstrate that the  Neurospora  homologue of  chd1  is required for normal remodeling of chromatin at  frq  and is required for normal  frq  expression and sustained rhythmicity. Surprisingly, our studies of CHD1 also revealed that DNA sequences within the  frq  promoter are methylated, and deletion of  chd1  results in expansion of this methylated domain. DNA methylation of the  frq  locus is altered in strains bearing mutations in a variety of circadian clock genes, including  frq ,  frh ,  wc-1 , and the gene encoding the  frq  antisense transcript ( qrf ). Furthermore,  frq  methylation depends on the DNA methyltransferase, DIM-2. Phenotypic characterization of  Δdim-2  strains revealed an approximate WT period length and a phase advance of approximately 2 hours, indicating that methylation plays only an ancillary role in clock-regulated gene expression. This suggests that DNA methylation, like the antisense transcript, is necessary to establish proper clock phasing but does not control overt rhythmicity. These data demonstrate that the epigenetic state of clock genes is dependent on normal regulation of clock components.

CHD1 Remodels Chromatin and Influences Transient DNA Methylation at the Clock Gene frequency