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Feedback control of Set1 protein levels is important for proper H3K4 methylation patterns

ABSTRACT: Methylation of histone H3 lysine 4 by the Set1 subunit of COMPASS correlates withactive transcription. Here we show that Set1 levels are regulated by protein degradation in response to multiple signals. Set1 levels are greatly reduced when COMPASS recruitment to genes, H3K4 methylation, or transcription is blocked. The degradation sequences map to N-terminal regions that overlap a previously identified auto-inhibitory domain, as well as the catalytic domain. Truncation mutants of Set1 that cause under- or over-expression produce abnormal H3K4 methylation patterns on transcribed genes. Surprisingly, SAGA-dependent genes are more strongly affected than TFIID-dependent genes, reflecting differences in their chromatin dynamics. We propose that careful tuning of Set1 levels by regulated degradation is critical for establishment and maintenance of proper H3K4 methylation patterns.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE55082 | GEO | 2014/02/28

SECONDARY ACCESSION(S): PRJNA238478

REPOSITORIES: GEO

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Feedback control of Set1 protein levels is important for proper H3K4 methylation patterns

Project description:Methylation of histone H3 lysine 4 by the Set1 subunit of COMPASS correlates withactive transcription. Here we show that Set1 levels are regulated by protein degradation in response to multiple signals. Set1 levels are greatly reduced when COMPASS recruitment to genes, H3K4 methylation, or transcription is blocked. The degradation sequences map to N-terminal regions that overlap a previously identified auto-inhibitory domain, as well as the catalytic domain. Truncation mutants of Set1 that cause under- or over-expression produce abnormal H3K4 methylation patterns on transcribed genes. Surprisingly, SAGA-dependent genes are more strongly affected than TFIID-dependent genes, reflecting differences in their chromatin dynamics. We propose that careful tuning of Set1 levels by regulated degradation is critical for establishment and maintenance of proper H3K4 methylation patterns. Genome binding/occupancy profiling of H3K4me2 and H3K4me3 in yeast

2014-02-28 | E-GEOD-55082 | biostudies-arrayexpress

The Set1 N-terminal domain and Swd2 interact with the RNA polymerase II CTD to recruit COMPASS

Project description:Methylation of histone H3 lysine 4 (H3K4) by the Set1/COMPASS complex is coupled with active transcription, and this modification is important for regulating gene expression. Set1/COMPASS associates with the RNA polymerase II (RNApII) C-terminal domain (CTD) to establish proper levels and distribution of H3K4 methylations.To ask how the Set1-RNApII CTD binding affects the occupancy and overall level of H3K4 methylations, ChIP-Seq was pefromed in cells transformed with full length or N-terminal truncated Set1. Our results indicate that Set1-RNApII CTD interaction is necessary for maintaining H3K4 methylations throughout the genes.

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Context Dependency of Set1/COMPASS Mediated H3 Lysine 4 Trimethylation

Project description:The stimulation of trimethylation of histone H3 lysine 4 (H3K4) by H2B monoubiquitination (H2Bub) has been widely studied with multiple mechanisms proposed for this form of histone crosstalk. Cps35/Swd2 within COMPASS is considered to bridge these processes. However, a truncated form of Set1 (762-Set1) is reported to function in H3K4 trimethylation without interacting with Cps35/Swd2, and such crosstalk is attributed to the n-SET domain of Set1 and its interaction with the Cps40/Spp1 subunit of COMPASS. Here, we use biochemical, structural, in vivo, and ChIP-seq approaches to demonstrate that Cps40/Spp1 and the n-SET domain of Set1 are required for the stability of Set1 and not the crosstalk. Furthermore, the apparent wild-type levels of H3K4 trimethylation (H3K4me3) in the 762-Set1 strain is due to rogue methylase activity of this mutant resulting in the mislocalization of H3K4me3 from the promoter-proximal regions to gene bodies and intergenic regions. We have also performed detailed screens and identified yeast strains lacking H2Bub, but containing intact H2Bub enzymes, that have normal levels of H3K4me3, suggesting that ubiquitination may not directly stimulate COMPASS, but rather works in a context of the PAF and Rad6/Bre1 complexes. Our study demonstrates that the ubiquitination machinery and Cps35/Swd2 function to focus COMPASS’ H3K4me3 activity at promoter-proximal regions in a context dependent manner. ChIP-Seq for H3K4ME3 in S. cerevisie wild-type strains and strains expressing a truncated form of Set1: aa762-1080 Set1. H3K4ME3 ChIP-Seq was also compared for wild-type, leo1 knockout, and chd1 knockout strains

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N-terminal acetylation of the Set1-COMPASS fine-tunes H3K4 methylation patterns (ChIPseq for Set1 occupancy in ard1 deletion strain)

Project description:H3K4 methylation is a conserved histone modification crucial for gene regulation, yet the post-translational modifications of the Set1-COMPASS complex remain largely unexplored. This study elucidates the significance of N-terminal acetylation in modulating H3K4 methylation patterns. Firstly, loss of NatA complex resulted in a significant decrease in H3K4me3 levels and a shift of H3K4me2 from 5' transcribed regions to promoters. Importantly, NatA physically interacted with the Set1-COMPASS complex and facilitated N-terminal acetylation of the Shg1 subunit. Surprisingly, deletion of SHG1 or mutation of the acetylation site (A2P) in Shg1 led to reduced H3K4 methylation in cells lacking Spp1. Additionally, NatB complex also contributed to H3K4 methylation regulation, potentially through N-terminal acetylation of Swd1. These findings highlight the novel role of N-terminal acetylation in fine-tuning the function of the Set1-COMPASS complex and shaping H3K4 methylation patterns. This study sheds light on the intricate regulation of H3K4 methylation and emphasizes the significance of N-terminal acetylation as a regulatory mechanism in this process.

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Context Dependency of Set1/COMPASS Mediated H3 Lysine 4 Trimethylation

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N-terminal acetylation of the Set1-COMPASS fine-tunes H3K4 methylation patterns (ChIPseq for shg1 and spp1 deletion strains)

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Mass spectrometry-based characterization of SET1/COMPASS complex in Caenorhabditis elegans

Project description:Changes in histone post-translational modifications are associated with aging through poorly defined mechanisms. Histone 3 lysine 4 (H3K4) methylation at promoters is deposited by SET1 family methyltransferases acting within conserved multiprotein complexes known as COMPASS. Using co-immunopurification coupled to mass spectrometry-based proteomics, we characterized complex members and binding partners in various genetic contexts, using WDR-5 or CFP-1 proteins as baits.

2021-12-08 | PXD029904 | Pride

Swd2/Cps35 determines H3K4 tri-methylation via interactions with Set1 and Rad6_Chromatin occupancy of Set1 in several strains

Project description:Histone H3K4 tri-methylation (H3K4me3) catalyzed by Set1/COMPASS, is a prominent epigenetic mark found in promoter-proximal regions of actively transcribed genes. H3K4me3 relies on prior monoubiquitination at the histone H2B (H2Bub) by Rad6 and Bre1. Swd2/Cps35, a Set1/COMPASS component, has been proposed as a key player in facilitating H2Bub-dependent H3K4me3. However, a more comprehensive investigation regarding the relationship among Rad6, Swd2 and Set1 is required to further understand the mechanisms and functions of the H3K4 methylation. We investigated the genome-wide occupancy patterns of Rad6, Swd2 and Set1 under various genetic conditions, aiming to clarify the roles of Set1 and Rad6 for occupancy of Swd2. Swd2 peaks appear on both 5’region and 3’region of genes, which are overlapped with its tightly bound two complexes, Set1 and CPF (Cleavage and Polyadenylation Factor), respectively. In the absence of Rad6/H2Bub, Set1 predominantly localized to the 5ʹ region of genes, while Swd2 lost all the chromatin binding. However, in the absence of Set1, Swd2 occupancy near the 5’region was impared and rather increased in the 3’ region. This study highlights that catalytic activity of Rad6 is essential for all the ways of Swd2’s binding to the transcribed genes and Set1 redistributes the Swd2 to 5’region for accomplishments of H3K4me3 in the genome-wide level.

2024-04-21 | GSE234564 | GEO

Transcriptional regulation by Set1 H3K4 methyltransferase and Jhd2 H3K4 demethylase

Project description:Histone H3K4 methylation is connected to gene transcription from yeast to humans, but its mechanistic role in transcription and chromatin dynamics remains poorly understood. Here, we investigated the functions for Set1 and Jhd2, the sole H3K4 methyltransferase and H3K4 demethylase, respectively, in S. cerevisiae. Our data show that Set1 and Jhd2 predominantly co-regulate transcription. To further understand the role for H3K4 methylation, we overexpressed Flag epitope-tagged SET1-G990E (a dominant hyperactive allele of SET1) in yeast using the constitutive ADH1 promoter (ADH1p). As a control, we also overexpressed Flag epitope-tagged wild type SET1 in yeast. Analysis of gene expression in set1-null, jhd2-null and wild type SET1 or hypeactive SET1-G990E overexpressing mutants together revealed that the transcriptional regulation at a sub-set of genes, inclduing those governing glycogen metabolism and ribosome biogenesis, is highly sensitive to any change (i.e., loss or gain) in H3K4 methylation levels. Overall, we find combined activities of Set1 and Jhd2 via dynamic modulation of H3K4 methylation contribute to positive or negative transcriptional regulation at shared target genes.

2016-06-15 | GSE73406 | GEO

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