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Interferon stimulation creates chromatin marks to establish transcriptional memory

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE89440 | GEO | 2018/08/28

REPOSITORIES: GEO

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Interferon stimulation creates chromatin marks and establishes transcriptional memory.

Project description:Epigenetic memory for signal-dependent transcription has remained elusive. So far, the concept of epigenetic memory has been largely limited to cell-autonomous, preprogrammed processes such as development and metabolism. Here we show that IFNβ stimulation creates transcriptional memory in fibroblasts, conferring faster and greater transcription upon restimulation. The memory was inherited through multiple cell divisions and led to improved antiviral protection. Of ∼2,000 IFNβ-stimulated genes (ISGs), about half exhibited memory, which we define as memory ISGs. The rest, designated nonmemory ISGs, did not show memory. Surprisingly, mechanistic analysis showed that IFN memory was not due to enhanced IFN signaling or retention of transcription factors on the ISGs. We demonstrated that this memory was attributed to accelerated recruitment of RNA polymerase II and transcription/chromatin factors, which coincided with acquisition of the histone H3.3 and H3K36me3 chromatin marks on memory ISGs. Similar memory was observed in bone marrow macrophages after IFNγ stimulation, suggesting that IFN stimulation modifies the shape of the innate immune response. Together, external signals can establish epigenetic memory in mammalian cells that imparts lasting adaptive performance upon various somatic cells.

| S-EPMC6166839 | biostudies-other

Interferon stimulation creates chromatin marks to establish transcriptional memory

Project description:Interferon stimulation creates chromatin marks to establish transcriptional memory

| PRJNA352210 | ENA

STAT1 is required to establish but not maintain interferon-γ-induced transcriptional memory

Project description:Exposure of human cells to interferon-γ (IFNγ) results in a mitotically heritable yet reversible state called long-term transcriptional memory. We previously identified the clustered GBP genes as strongly primed by IFNγ. Here we discovered that in primed cells, both interferon-responsive transcription factors STAT1 and IRF1 target chromatin with accelerated kinetics upon re-exposure to IFNγ, specifically at promotors of primed genes. Priming does not alter the degree of IFNγ-induced STAT1 activation or nuclear import, indicating that memory does not alter upstream JAK-STAT signalling. We found STAT1 to be critical to establish transcriptional memory but in a manner that is independent of mere transcription activation. Interestingly, while Serine 727 phosphorylation of STAT1 was maintained during the primed state, STAT1 is not required for the heritability of GBP gene memory. Our results suggest that memory of interferon exposure constitutes a STAT1-mediated, heritable state that is established during priming. This renders GBP genes poised for subsequent STAT1 and IRF1 binding and accelerated gene activation upon a secondary interferon exposure.

| S-SCDT-10_15252-EMBJ_2022112259 | biostudies-other

Chrom-seq Identifies RNAs at Chromatin Marks

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-31 | GSE252810 | GEO

A transcription factor pulse can prime chromatin for heritable transcriptional memory

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-12-21 | GSE72488 | GEO

The chromatin remodeler RSF1 coordinates epigenetic marks for transcriptional repression and DSB repair.

Project description:DNA lesions impact on local transcription and the damage-induced transcriptional repression facilitates efficient DNA repair. However, how chromatin dynamics cooperates with these two events remained largely unknown. We here show that histone H2A acetylation at K118 is enriched in transcriptionally active regions. Under DNA damage, the RSF1 chromatin remodeling factor recruits HDAC1 to DSB sites. The RSF1-HDAC1 complex induces the deacetylation of H2A(X)-K118 and its deacetylation is indispensable for the ubiquitination of histone H2A at K119. Accordingly, the acetylation mimetic H2A-K118Q suppressed the H2A-K119ub level, perturbing the transcriptional repression at DNA lesions. Intriguingly, deacetylation of H2AX at K118 also licenses the propagation of γH2AX and recruitment of MDC1. Consequently, the H2AX-K118Q limits DNA repair. Together, the RSF1-HDAC1 complex controls the traffic of the DNA damage response and transcription simultaneously in transcriptionally active chromatins. The interplay between chromatin remodelers and histone modifiers highlights the importance of chromatin versatility in the maintenance of genome integrity.

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Parsing the interferon transcriptional network and its disease associations

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-24 | E-GEOD-75306 | biostudies-arrayexpress

Histone retention preserves epigenetic marks during heat stress-induced transcriptional memory in plants

Project description:Plants often experience recurrent stressful events, for example during heat waves. They can be primed by heat stress (HS) to improve survival of more severe heat stress conditions. At certain genes, sustained expression is induced for several days beyond the initial heat stress. This transcriptional memory is associated with hyper-methylation of histone H3 lysine 4 (H3K4me3), but it is unclear how this is maintained for extended periods. Here, we determined histone turnover by measuring chromatin association of HS-induced histone H3.3. Genome-wide histone turnover was not homogenous, in particular, H3.3 was retained longer at heat stress-memory genes compared to HS-induced non-memory genes during the memory phase. While low nucleosome turnover retained H3K4 methylation, methylation loss did not affect turnover, suggesting that low nucleosome turnover sustains H3K4 methylation, but not vice versa. Together, our results unveil the modulation of histone turnover as a mechanism to retain environmentally-mediated epigenetic modifications.

| S-SCDT-10_15252-EMBJ_2023113595 | biostudies-other

CD4+ T-cell help creates effector memory CTLs with innate and help-independent recall capacities

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-23 | GSE118160 | GEO

A hyperactive transcriptional state marks genome reactivation at the mitosis-G1 transition

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-15 | E-GEOD-83293 | biostudies-arrayexpress