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Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE231521 | GEO | 2023/05/04

REPOSITORIES: GEO

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Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ThioU]

Project description:Current models posit that nuclear speckles (NSs) serve as reservoirs of splicing factors and facilitate post-transcriptional processing of mRNA. Here, we discovered that ribotoxic stress leads to a profound reorganization of NSs with enhanced recruitment of factors required for 5' and 3' splice site recognition including the RNA-binding protein TIAR, U1 snRNP proteins and U2-associated factor 65, as well as serine 2 phosphorylated RNA polymerase II. NS reorganization is dependent on the stress-activated p38 mitogen activated protein kinase (MAPK), and goes along with splicing activation of both pre-existing and nascent pre-mRNAs. In particular, ribotoxic stress causes targeted excision of retained introns from pre-mRNAs of immediate early genes (IEGs), whose transcription is induced during the stress response. Importantly, enhanced splicing of the IEGs ZFP36 and FOS is accompanied by re-localization of the corresponding mRNAs to NSs. Our study reveals NSs as a dynamic compartment that is remodeled under stress conditions to promote the excision of retained introns and thereby enhance the expression and processing of IEG mRNAs.

2023-05-04 | GSE231520 | GEO

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [HLs]

2023-05-04 | GSE231519 | GEO

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ANI]

2021-08-06 | GSE181446 | GEO

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization

Project description:Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization

| PRJNA966192 | ENA

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ThioU]

Project description:Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ThioU]

| PRJNA966199 | ENA

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [HLs]

Project description:Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [HLs]

| PRJNA966200 | ENA

Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ANI]

Project description:Stress-induced splicing activation of immediate early genes by nuclear speckle reorganization [ANI]

| PRJNA752091 | ENA

Stress induced gene expression: a direct role for MAPKAP kinases in transcriptional activation of immediate early genes.

Project description:Immediate early gene (IEG) expression is coordinated by multiple MAP kinase signaling pathways in a signal specific manner. Stress-activated p38? MAP kinase is implicated in transcriptional regulation of IEGs via MSK-mediated CREB phosphorylation. The protein kinases downstream to p38, MAPKAP kinase (MK) 2 and MK3 have been identified to regulate gene expression at the posttranscriptional levels of mRNA stability and translation. Here, we analyzed stress-induced IEG expression in MK2/3-deficient cells. Ablation of MKs causes a decrease of p38? level and p38-dependent IEG expression. Unexpectedly, restoration of p38? does not rescue the full-range IEG response. Instead, the catalytic activity of MKs is necessary for the major transcriptional activation of IEGs. By transcriptomics, we identified MK2-regulated genes and recognized the serum response element (SRE) as a common promoter element. We show that stress-induced phosphorylation of serum response factor (SRF) at serine residue 103 is significantly reduced and that induction of SRE-dependent reporter activity is impaired and can only be rescued by catalytically active MK2 in MK2/3-deficient cells. Hence, a new function of MKs in transcriptional activation of IEGs via the p38?-MK2/3-SRF-axis is proposed which probably cooperates with MKs' role in posttranscriptional gene expression in inflammation and stress response.

| S-EPMC3074129 | biostudies-literature

LSD1 modulates stress-evoked transcription of immediate early genes and emotional behavior.

Project description:Behavioral changes in response to stressful stimuli can be controlled via adaptive epigenetic changes in neuronal gene expression. Here we indicate a role for the transcriptional corepressor Lysine-Specific Demethylase 1 (LSD1) and its dominant-negative splicing isoform neuroLSD1, in the modulation of emotional behavior. In mouse hippocampus, we show that LSD1 and neuroLSD1 can interact with transcription factor serum response factor (SRF) and set the chromatin state of SRF-targeted genes early growth response 1 (egr1) and c-fos Deletion or reduction of neuro LSD1 in mutant mice translates into decreased levels of activating histone marks at egr1 and c-fos promoters, dampening their psychosocial stress-induced transcription and resulting in low anxiety-like behavior. Administration of suberoylanilide hydroxamine to neuroLSD1(KO)mice reactivates egr1 and c-fos transcription and restores the behavioral phenotype. These findings indicate that LSD1 is a molecular transducer of stressful stimuli as well as a stress-response modifier. Indeed, LSD1 expression itself is increased acutely at both the transcriptional and splicing levels by psychosocial stress, suggesting that LSD1 is involved in the adaptive response to stress.

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NR4A1 regulates expression of immediate early genes, suppressing replication stress in cancer.

Project description:Deregulation of oncogenic signals in cancer triggers replication stress. Immediate early genes (IEGs) are rapidly and transiently expressed following stressful signals, contributing to an integrated response. Here, we find that the orphan nuclear receptor NR4A1 localizes across the gene body and 3' UTR of IEGs, where it inhibits transcriptional elongation by RNA Pol II, generating R-loops and accessible chromatin domains. Acute replication stress causes immediate dissociation of NR4A1 and a burst of transcriptionally poised IEG expression. Ectopic expression of NR4A1 enhances tumorigenesis by breast cancer cells, while its deletion leads to massive chromosomal instability and proliferative failure, driven by deregulated expression of its IEG target, FOS. Approximately half of breast and other primary cancers exhibit accessible chromatin domains at IEG gene bodies, consistent with this stress-regulatory pathway. Cancers that have retained this mechanism in adapting to oncogenic replication stress may be dependent on NR4A1 for their proliferation.

| S-EPMC8549465 | biostudies-literature

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