Neurospora
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192863 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR770463.fastq.gz | Fastqsanger.gz | |||
| SRR770465.fastq.gz | Fastqsanger.gz | |||
| SRR770466.fastq.gz | Fastqsanger.gz | |||
| SRR770467.fastq.gz | Fastqsanger.gz | |||
| SRR770468.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Heterochromatin is a specialized form of chromatin that restricts access to DNA and inhibits genetic processes, including transcription and recombination. In Neurospora crassa, constitutive heterochromatin is characterized by trimethylation of lysine 9 on histone H3, hypoacetylation of histones, and DNA methylation. Here we explore whether the conserved histone demethylase, lysine-specific demethylase 1 (LSD1), regulates heterochromatin in Neurospora, and if so, how. Though LSD1 is implicated in heterochromatin regulation, its function is inconsistent across different systems; orthologs of LSD1 have been shown to either promote or antagonize heterochromatin expansion by removing H3K4me or H3K9me respectively. We identify three members of the Neurospora LSD complex (LSDC): LSD1, PHF1, and BDP-1, and strains deficient for any exhibit variable spreading of heterochromatin and establishment of new heterochromatin domains dispersed across the genome. Heterochromatin establishment outside of canonical domains in Neurospora share the unusual characteristic of DNA methylation-dependent H3K9me3; typically, H3K9me3 establishment is independent of DNA methylation. Consistent with this, the hyper-H3K9me3 phenotype of LSD1 knock-out strains is dependent on the presence of DNA methylation, as well as HCHC-mediated histone deacetylation, suggesting spreading is dependent on some feedback mechanism. Altogether, our results suggest LSD1 works in opposition to HCHC to maintain proper heterochromatin boundaries.
2021-07-21 | PXD017300 | Pride
Project description:Repression of facultative heterochromatin is essential for developmental processes in numerous organisms. Methylation of histone H3 lysine 27 (H3K27) by Polycomb repressive complex 2 is a prominent feature of facultative heterochromatin in both fungi and higher eukaryotes. Although this methylation is frequently crucial for silencing, the detailed mechanism of repression remains poorly understood. We utilized a forward genetics approach to identify three previously uncharacterized genes required to maintain silencing at facultative heterochromatin genes in Neurospora crassa: sds3 (NCU01599), rlp1 (RPD3L protein 1; NCU09007) and rlp2 (RPD3L protein 2; NCU02898). We found that SDS3, RLP1, and RLP2 associate with N. crassa homologs of the Saccharomyces cerevisiae RPD3L complex and are required for repression of a subset of H3K27-methylated genes. Loss of these genes does not lead to loss of H3K27 methylation but increases acetylation of histone H3 lysine 14 at upregulated genes, and SDS3 binding levels are highest at genes derepressed upon loss of sds3, rlp1, and rlp2, implying that RPD3L-driven deacetylation is a previously undescribed factor required for silencing of facultative heterochromatin in N. crassa.
2024-08-21 | GSE261327 | GEO
Project description:Repression of facultative heterochromatin is essential for developmental processes in numerous organisms. Methylation of histone H3 lysine 27 (H3K27) by Polycomb repressive complex 2 is a prominent feature of facultative heterochromatin in both fungi and higher eukaryotes. Although this methylation is frequently crucial for silencing, the detailed mechanism of repression remains poorly understood. We utilized a forward genetics approach to identify three previously uncharacterized genes required to maintain silencing at facultative heterochromatin genes in Neurospora crassa: sds3 (NCU01599), rlp1 (RPD3L protein 1; NCU09007) and rlp2 (RPD3L protein 2; NCU02898). We found that SDS3, RLP1, and RLP2 associate with N. crassa homologs of the Saccharomyces cerevisiae RPD3L complex and are required for repression of a subset of H3K27-methylated genes. Loss of these genes does not lead to loss of H3K27 methylation but increases acetylation of histone H3 lysine 14 at upregulated genes, and SDS3 binding levels are highest at genes derepressed upon loss of sds3, rlp1, and rlp2, implying that RPD3L-driven deacetylation is a previously undescribed factor required for silencing of facultative heterochromatin in N. crassa.
2024-08-21 | GSE261325 | GEO
Project description:Development in higher organisms requires selective gene silencing, directed in part by di-/tri-methylation of lysine 27 on histone H3 (H3K27me2/3). Knowledge of the cues that control formation of such repressive Polycomb domains is extremely limited. We exploited natural and engineered chromosomal rearrangements in the fungus Neurospora crassa to elucidate the control of H3K27me2/3. Analyses of H3K27me2/3 in strains bearing chromosomal rearrangements revealed both position-dependent and position-independent facultative heterochromatin. We found that proximity to chromosome ends is necessary to maintain, and sufficient to induce, transcriptionally repressive, subtelomeric H3K27me2/3. We ascertained that such telomere-proximal facultative heterochromatin requires native telomere repeats and found that a short array of ectopic telomere repeats, (TTAGGG)17, can induce a large domain (~225 kb) of H3K27me2/3. This provides an example of a cis-acting sequence that directs H3K27 methylation. Our findings provide new insight into the relationship between genome organization and control of heterochromatin formation.
2017-12-29 | GSE104019 | GEO
Project description:Repression of facultative heterochromatin is essential for developmental processes in numerous organisms. Methylation of histone H3 lysine 27 (H3K27) by Polycomb repressive complex 2 is a prominent feature of facultative heterochromatin in both fungi and higher eukaryotes. Although this methylation is frequently crucial for silencing, the detailed mechanism of repression remains poorly understood. We utilized a forward genetics approach to identify three previously uncharacterized genes required to maintain silencing at facultative heterochromatin genes in Neurospora crassa: sds3 (NCU01599), rlp1 (RPD3L protein 1; NCU09007) and rlp2 (RPD3L protein 2; NCU02898). We found that SDS3, RLP1, and RLP2 associate with N. crassa homologs of the Saccharomyces cerevisiae RPD3L complex and are required for repression of a subset of H3K27-methylated genes. Loss of these genes does not lead to loss of H3K27 methylation but increases acetylation of histone H3 lysine 14 at upregulated genes, and SDS3 binding levels are highest at genes derepressed upon loss of sds3, rlp1, and rlp2, implying that RPD3L-driven deacetylation is a previously undescribed factor required for silencing of facultative heterochromatin in N. crassa.
2024-08-21 | GSE261319 | GEO
Project description:Background: Regulation of chromatin accessibility and transcription are tightly coordinated processes. Studies in yeast and higher eukaryotes has described accessible chromatin regions, but little work has been done in filamentous fungi. Results: Here we present a genome-scale characterization of accessible chromatin regions in Neurospora crassa, which revealed characteristic molecular features of accessible and inaccessible chromatin. We present experimental evidence of inaccessibility within heterochromatin regions in Neurospora, and we examine features of both accessible and inaccessible chromatin, including the presence of histone modifications, types of transcription, transcription factor binding, and relative nucleosome turnover rates. Chromatin accessibility is not strictly correlated with expression level. Accessible chromatin regions in the model filamentous fungus Neurospora are characterized the presence of H3K27 acetylation and commonly associated with pervasive non-coding transcription. Conversely, methylation of H3 lysine-36 catalyzed by ASH1 is correlated with inaccessible chromatin within promoter regions. Conclusions: In N. crassa, H3K27 acetylation is the most predictive histone modification for open chromatin. Conversely, our data show that H3K36 methylation is a key marker of inaccessible chromatin in gene-rich regions of the genome. Our data are consistent with an expanded role for H3K36 methylation in intergenic regions of filamentous fungi compared to the model yeasts, S. cerevisiae and S. pombe, which lack homologs of the ASH1 methyltransferase. of accessible chromatin in Neurospora
2020-11-12 | GSE154497 | GEO
Project description:Formation of facultative heterochromatin by Polycomb Repressive Complex 2 (PRC2) is a well conserved epigenetic mechanism that functions to control transcriptional dynamics across eukaryotes. PRC2 catalyzes histone H3 lysine 27 tri-methylation (H3K27me3), a histone post-translational modification that helps maintain stable gene repression. Gene repression by PRC2 is important for organismal development and defects in PRC2 function are associated with human ailments, such as Weaver syndrome and various cancers. In this study, we reveal the replication-dependent histone chaperone, Chromatin Assembly Factor 1 (CAF-1), is required for normal facultative heterochromatin formation in model fungus N. crassa. CAF-1 deficiency results in widespread misregulation of gene expression, particularly within facultative heterochromatin domains, which is accompanied by a rearrangement of H3K27me3 patterns. Regional losses of H3K27me3 are associated with reduced levels of ASH-1 catalyzed H3K36 methylation, and gains of histone modifications associated with active transcription. Furthermore, analysis of a double mutant deficient for both CAF-1 and PRC2 activity revealed that these complexes play distinct roles in maintaining gene repression and facultative heterochromatin. Collectively, these results shed light on CAF-1's role in maintaining a repressive chromatin environment.
2025-12-26 | GSE314683 | GEO
Project description:Formation of facultative heterochromatin by Polycomb Repressive Complex 2 (PRC2) is a well conserved epigenetic mechanism that functions to control transcriptional dynamics across eukaryotes. PRC2 catalyzes histone H3 lysine 27 tri-methylation (H3K27me3), a histone post-translational modification that helps maintain stable gene repression. Gene repression by PRC2 is important for organismal development and defects in PRC2 function are associated with human ailments, such as Weaver syndrome and various cancers. In this study, we reveal the replication-dependent histone chaperone, Chromatin Assembly Factor 1 (CAF-1), is required for normal facultative heterochromatin formation in model fungus N. crassa. CAF-1 deficiency results in widespread misregulation of gene expression, particularly within facultative heterochromatin domains, which is accompanied by a rearrangement of H3K27me3 patterns. Regional losses of H3K27me3 are associated with reduced levels of ASH-1 catalyzed H3K36 methylation, and gains of histone modifications associated with active transcription. Furthermore, analysis of a double mutant deficient for both CAF-1 and PRC2 activity revealed that these complexes play distinct roles in maintaining gene repression and facultative heterochromatin. Collectively, these results shed light on CAF-1's role in maintaining a repressive chromatin environment.
2025-12-26 | GSE314682 | GEO
Project description:We report the application of cut&tag technology for high-throughput profiling of histone modifications Raji Epstein–Barr viral genome in reponse to bryostatin treatment. Dual- and tri-methylation of lysine 4 on histone H3 protein indicate genes that are actively expressed/regulated. Tri-methylation of lysine 27 on histone H3 protein marks genes that are negatively regulated or suppressed for expression.
2022-01-05 | GSE192837 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE28374: DNA methylation of miRNA genes in HMEC and HMF GSE28375: Histone H3 acetylation of miRNA genes in HMEC and HMF GSE28376: Histone H3 lysine 27 trimethylation of miRNA genes in HMEC and HMF GSE28377: Histone H3 lysine 4 trimethylation of miRNA genes in HMEC and HMF GSE28378: Histone H3 lysine 9 dimethylation of miRNA genes in HMEC and HMF Refer to individual Series
2011-04-05 | E-GEOD-28380 | biostudies-arrayexpress