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Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains

ABSTRACT: Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains

PROVIDER: PRJNA989169 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25074600.fastq.gz	Fastqsanger.gz
	SRR25074601.fastq.gz	Fastqsanger.gz
	SRR25074602.fastq.gz	Fastqsanger.gz
	SRR25074603.fastq.gz	Fastqsanger.gz
	SRR25074583.fastq.gz	Fastqsanger.gz

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Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains

Project description:Mechanisms enabling genetically identical cells to differentially regulate gene expression are complex and central to organismal development and evolution. While gene silencing pathways involving DNA sequence–specific recruitment of histone-modifying enzymes are prevalent in nature, examples of sequence-independent heritable gene silencing are scarce. Studies of the fission yeast Schizosaccharomyces pombe indicate that sequence-independent propagation of heterochromatin can occur but requires numerous multisubunit protein complexes and their diverse activities. Such complexity has so far precluded a coherent articulation of the minimal requirements for heritable gene silencing by conventional in vitro reconstitution approaches. Here, we take an unconventional approach to defining these requirements by engineering sequence-independent silent chromatin inheritance in budding yeast Saccharomyces cerevisiae cells. The mechanism conferring memory upon these cells is remarkably simple and requires only two proteins, one that recognizes histone H3 lysine 9 methylation (H3K9me) and catalyzes the deacetylation of histone H4 lysine 16 (H4K16), and another that recognizes deacetylated H4K16 and catalyzes H3K9me. Together, these bilingual “read–write” proteins form an interdependent positive feedback loop that is sufficient for the transmission of DNA sequence–independent silent information over multiple generations.

2023-12-19 | GSE236173 | GEO

Minimal requirements for the epigenetic inheritance of engineered silent chromatin domains.

Project description:Mechanisms enabling genetically identical cells to differentially regulate gene expression are complex and central to organismal development and evolution. While gene silencing pathways involving DNA sequence-specific recruitment of histone-modifying enzymes are prevalent in nature, examples of sequence-independent heritable gene silencing are scarce. Studies of the fission yeast Schizosaccharomyces pombe indicate that sequence-independent propagation of heterochromatin can occur but requires numerous multisubunit protein complexes and their diverse activities. Such complexity has so far precluded a coherent articulation of the minimal requirements for heritable gene silencing by conventional in vitro reconstitution approaches. Here, we take an unconventional approach to defining these requirements by engineering sequence-independent silent chromatin inheritance in budding yeast Saccharomyces cerevisiae cells. The mechanism conferring memory upon these cells is remarkably simple and requires only two proteins, one that recognizes histone H3 lysine 9 methylation (H3K9me) and catalyzes the deacetylation of histone H4 lysine 16 (H4K16), and another that recognizes deacetylated H4K16 and catalyzes H3K9me. Together, these bilingual "read-write" proteins form an interdependent positive feedback loop that is sufficient for the transmission of DNA sequence-independent silent information over multiple generations.

| S-EPMC10801849 | biostudies-literature

Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

Project description:The epigenetic process safeguards cell identity during cell division through the inheritance of appropriate gene expression profiles. We demonstrated previously that parental nucleosomes are inherited by the same chromatin domains during DNA replication only in the case of repressed chromatin. We now show that this specificity is conveyed by NPM1, a histone H3/H4 chaperone. Proteomic analyses of late S-phase chromatin revealed NPM1 in association with both H3K27me3, an integral component of facultative heterochromatin and MCM2, an integral component of the DNA replication machinery; moreover NPM1 interacts directly with PRC2 and with MCM2. Given that NPM1 is essential, the inheritance of repressed chromatin domains was examined anew using mESCs expressing an auxin-degradable version of endogenous NPM1. Upon NPM1 degradation, cells accumulated in S-phase of the cell-cycle and parental nucleosome inheritance from repressed chromatin domains was markedly compromised. Appropriate inheritance required the NPM1 acidic patches that function in chaperone activity, pointing to NPM1 being integral to the epigenetic process.

2022-04-27 | GSE183090 | GEO

Specialized replication of heterochromatin domains ensures self-templated chromatin assembly and epigenetic inheritance [ChIP-seq]

Project description:Heterochromatin domains defined by distinct histone methylation patterns are a major feature of mammalian genomes. Epigenetic pathways ensure stable heterochromatin inheritance through cell division to prevent the expression of lineage-inappropriate genes and defects in this process can lead to many diseases including cancer. Previous studies have shown that heterochromatin maintenance requires a critical threshold of methylated histones, but how modified parental histones are transferred to daughter strands during DNA replication is unclear. We find that heterochromatin domains are specialized replication zones enriched in replisome components, which load factors that help retain parental histones. This mechanism is further supported by the boundary elements surrounding the heterochromatin domains. DNA replication is thus coordinated with histone preservation to facilitate epigenetic inheritance of heterochromatin.

2024-02-02 | GSE242353 | GEO

Epigenetic inheritance uncoupled from sequence-specific recruitment

Project description:We used ChIP-seq to examine the requirements for inheritance of H3K9me at endogenous and ectopic loci.

2014-11-26 | GSE63304 | GEO

Epigenetic inheritance uncoupled from sequence-specific recruitment

Project description:We used ChIP-seq to examine the requirements for inheritance of H3K9me at endogenous and ectopic loci. H3K9me2 and H3K9me3 ChIP-seq in multiple S. pombe strains

2014-11-26 | E-GEOD-63304 | biostudies-arrayexpress

Identification of a novel, tunable interface in the S.pombe HP1 protein, Swi6, that underpins epigenetic inheritance.

Project description:HP1 proteins bind dynamically to H3K9 methylation and are essential for establishing and maintaining transcriptionally silent epigenetic states, known as heterochromatin. HP1 proteins can dimerize, forming a binding interface that interacts with and recruits diverse chromatin-associated factors. HP1 proteins rapidly evolve through sequence changes and gene duplications, but the extent of variation required to achieve functional specialization is unknown. To investigate how changes in amino acid sequence impact epigenetic inheritance, we performed a targeted mutagenesis screen of the dimerization and protein interaction domain of the S.pombe HP1 homolog Swi6. We discovered that substitutions mapping to an auxiliary motif in Swi6 outside the dimerization interface can lead to complete functional divergence. Specifically, we identified point mutations at a single amino acid residue that resulted in either persistent gain or loss of function in epigenetic inheritance without affecting heterochromatin establishment. These substitutions increase Swi6 chromatin occupancy in vivo and alter Swi6-protein interactions that selectively affect H3K9me inheritance. Based on our findings, we propose that relatively minor changes in Swi6 amino acid composition can lead to profound changes in epigenetic inheritance, underscoring the remarkable plasticity associated with HP1 proteins and their ability to evolve new functions.

2024-08-10 | PXD047651 | Pride

Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

Project description:Inheritance of Repressed Chromatin Domains during S-phase Requires the Histone Chaperone NPM1

| PRJNA759176 | ENA

Specialized replication of heterochromatin domains ensures self-templated chromatin assembly and epigenetic inheritance

Project description:Specialized replication of heterochromatin domains ensures self-templated chromatin assembly and epigenetic inheritance

| PRJNA1013416 | ENA

The chromatin modifiers SET-25 and SET-32 are required for initiation but not long-term maintenance of transgenerational epigenetic inheritance

Project description:Some epigenetic modifications are inherited from one generation to the next, providing a potential mechanism for the inheritance of environmentally acquired traits. Transgenerational inheritance of RNA interference phenotypes in C. elegans provides an excellent model to study this phenomenon, and whilst studies have implicated both chromatin modifications and small RNA pathways in heritable silencing their relative contributions remain unclear. Here we demonstrate that the histone methyltransferases SET-25 and SET-32 are required for the establishment of a transgenerational silencing signal, but not for long-term maintenance of this signal between subsequent generations suggesting that transgenerational epigenetic inheritance is a multi-step process, with distinct genetic requirements for establishment and maintenance of heritable silencing. Furthermore, small RNA sequencing reveals that the abundance of secondary siRNA (thought to be the effector molecules of heritable silencing) does not correlate with silencing phenotypes. Together, our results suggest that the current mechanistic models of epigenetic inheritance are incomplete.

2018-10-30 | PXD008754 | Pride

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