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Set1 is a critical transcriptional regulator in response to external signals

ABSTRACT: Set1-mediated methylation of histone H3 at lysine 4 (H3K4) is a well-established marker of active transcription in eukaryotes. However, absence of Set1 did not significantly alter the overall gene expression; interestingly, some genes exhibited enhanced expression in Candida albicans. The present study aimed to elucidate the role of Set1 in transcription of genes that exhibited increased expression levels in its absence. Ideally, these genes should be repressed and activated in response to specific signals. The hypha-specific genes of C. albicans were expressed in the absence of Set1, even without any external activating signals. These inducible genes displayed atypical H3K4 modification patterns. During the initial induction stages, H3K4 methylation was not involved in the rapid and explosive expression of these genes; instead, acetylation of the same residue was involved. H3K4 acetylation significantly increased in the absence of H3K4 methylation, allowing genes that did not receive external transcriptional signals to initiate mRNA expression, leading to morphological changes. With continued exposure to induction signals, the heightened H3K4 acetylation decreased while H3K4 methylation increased in these genes. Thus, inducible genes receive a positive feedback for stable and sustainable expression. In conclusion, Set1 is a key regulator of transcription in response to external environment changes.

ORGANISM(S): Mus musculus

PROVIDER: GSE247148 | GEO | 2025/07/16

REPOSITORIES: GEO

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Set1 is a critical transcriptional regulator in response to external signals [ChIP-seq]

Project description:Set1-mediated methylation of histone H3 at lysine 4 (H3K4) is a well-established marker of active transcription in eukaryotes. However, absence of Set1 did not significantly alter the overall gene expression; interestingly, some genes exhibited enhanced expression in Candida albicans. The present study aimed to elucidate the role of Set1 in transcription of genes that exhibited increased expression levels in its absence. Ideally, these genes should be repressed and activated in response to specific signals. The hypha-specific genes of C. albicans were expressed in the absence of Set1, even without any external activating signals. These inducible genes displayed atypical H3K4 modification patterns. During the initial induction stages, H3K4 methylation was not involved in the rapid and explosive expression of these genes; instead, acetylation of the same residue was involved. H3K4 acetylation significantly increased in the absence of H3K4 methylation, allowing genes that did not receive external transcriptional signals to initiate mRNA expression, leading to morphological changes. With continued exposure to induction signals, the heightened H3K4 acetylation decreased while H3K4 methylation increased in these genes. Thus, inducible genes receive a positive feedback for stable and sustainable expression. In conclusion, Set1 is a key regulator of transcription in response to external environment changes.

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Project description:Candida albicans is an opportunistic human fungal pathogen. It exists as a member of human normal flora but can cause infection in immunocompromised individuals. Transition to pathogenic C. albicans requires a change in gene expression of various genes. As the histone-modifying enzymes can regulate gene expression, they can be considered as a factor controlling the virulence of C. albicans. Among them, it has been reported that the absence of H3K4 methyltransferase Set1 reduces the virulence of C. albicans. However, Set1-regulated genes responsible for this attenuated virulence phenotype are unknown. Here, we identified that the Set1 positively regulates the expression of mitochondrial protein genes and oxidative stress response-related genes through the methylation of H3K4. Levels of cellular mitochondrial reactive oxygen species (ROS) in Δset1 are also higher than those in the wild-type. Furthermore, Set1 deletion increases sensitivity to hydrogen peroxide (H2O2). Set1 deleted mutant also does not form its colony properly when it interacts with macrophage in vitro, in agreement with its attenuated virulence in vivo. Therefore, Set1 is required to inhibit cellular ROS production by positive regulation of mitochondrial protein genes and oxidative stress response-related genes expression, and consequently, the Set1-mediated gene expression assists C. albicans in defending against ROS generated from the host more rapidly.

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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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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

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

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Differentially expressed genes in absence of histone H3K4 methyltransferase Set1 in Candida albicans

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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.

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