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The Chromatin Remodeler, Mit1, Enables the Propagation of the Histone Modification, H3K9me [RNA-seq]

ABSTRACT: Chromatin structure dynamically regulates the balance between DNA accessibility and compaction, which is essential for controlling gene expression in eukaryotic cells. ATP-dependent chromatin remodelers are key effectors in this process, modulating nucleosome positioning to establish either open or repressive chromatin states. The CHD family of remodelers exhibits diverse roles in transcriptional regulation, yet the mechanisms by which they contribute to transcriptional silencing remain incompletely understood. In Schizosaccharomyces pombe, the CHD remodeler Mit1 functions within the SHREC complex to enforce heterochromatin formation, but its precise mode of action is unclear. Here, we directly tether Mit1 to an ectopic chromatin locus and demonstrate that Mit1 recruitment induces transcriptional gene silencing and nucleates broad domains of H3K9 methylation in a manner dependent on the Clr4 methyltransferase. This silencing requires Mit1’s remodeling activity but does not involve direct physical interaction with Clr4, indicating that Mit1 remodels chromatin to create a substrate favorable for Clr4 function. Furthermore, we find that enables the formation of de novo heterochromatin domains genome-wide. Our findings uncover a novel feedback mechanism whereby CHD-family remodelers initiate stable heterochromatin formation through chromatin remodeling that promotes methylation-based silencing, revealing new insights into the interplay between nucleosome dynamics and epigenetic gene regulation.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE325547 | GEO | 2026/03/31

REPOSITORIES: GEO

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	GSE325547_gene_counts_matrix_GEO.txt.gz	Txt

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Project description:Abstract: In the yeast S. pombe, multiple chromatin-modifying enzymes are required for heterochromatin formation, yet how their actions alter chromatin structure to block access to DNAby the transcriptional machinery is unknown. We constructed high-resolution nucleosome occupancy maps of heterochromatic regions in wild-type strains and in mutants lacking the H3K9 methyltransferase Clr4 or one of the two activities of the silencing effector complex SHREC. Fourier analysis reveals that these enzymes do not increase the regularity of nucleosome spacing. Rather, their principal effect was to induce the elimination of nucleosome-free regions (NFRs). Both NFRs associated with transcription initiation sites as well as those not associated with promoters are affected. As in S. cerevisiae, repressed genes in euchromatin retain their NFRs. Thus, NFR elimination cannot be explained as a secondary consequence of repression. The maps also show that TFIIIC boundary elements have NFRs resistant to silencing, suggesting a potential role in preventing lateral spread of heterochromatin. NFR elimination offers a mechanism by which heterochromatin restricts access of the transcriptional machinery to DNA. Nucleosome positions in either heterochromatin or euchromatin were mapped in various mutants to determine whether chromatin structure is altered upon heterochromatic silencing. Eight strains were assayed for nucleosome positioning in heterochromatin while two strains were assayed for nucleosome positioning in euchromatin. Two biological replicates were assayed for each strain. No dye swaps were done. RNA transcripts were also mapped using the heterochromatin tiling arrays to determine where RNA transcripts accumulate in heterochromatin. Three strains were assayed for transcripts in heterochromatin by hybridizing cy5-labeled cDNA created from total RNA against cy3-labeled cDNA created from RNA synthesized from sonicated genomic DNA. Two biological replicates were assayed for each strain.

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The Chromatin Remodeler, Mit1, Enables the Propagation of the Histone Modification, H3K9me [RNA-seq]

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