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

ABSTRACT: Histone retention preserves epigenetic marks during heat stress-induced transcriptional memory

PROVIDER: PRJNA902769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22324721_1.fastq.gz	Fastqsanger.gz
	SRR22324721_2.fastq.gz	Fastqsanger.gz
	SRR22324722_1.fastq.gz	Fastqsanger.gz
	SRR22324722_2.fastq.gz	Fastqsanger.gz
	SRR22324723_1.fastq.gz	Fastqsanger.gz

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

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

2023-10-18 | GSE218234 | GEO

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 the 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 the 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-EPMC10711655 | biostudies-literature

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.

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Project description:A total of 3,851 proteins were detected, with quantitative information available for 3,835 proteins. Among these, we identified 1,423 differentially abundant proteins (DAPs), including 526 proteins that were classified as Heat Stress Memory Proteins (HSMPs). GO and KEGG enrichment analyses revealed that the HSMPs were primarily associated with the "autophagy" in R4 and with "PSII repair", "HSP binding", and "peptidase activity" in S5. Notably, we identified 7 chloroplast-localized HSMPs (HSP21, DJC77, EGY3, LHCA4, LQY1, PSBR and DEGP8, R4/S0>1.2, S5/S0>1.2), which were considered to be effectors linked to PSII heat stress memory, predominantly in cluster 4. Protein-protein interaction (PPI) analysis indicated that the ubiquitin-proteasome system, with key nodes at UPL3, RAD23b, and UCH3, might play a role in the selective retention of memory effectors in the R4 stage.These findings provide valuable insights into the establishment of heat stress memory under recurring high-temperature episodes and offer a conceptual framework for breeding thermotolerant crops with improved PSII functionality.

2024-06-26 | PXD053448 |

Transcriptomic analysis of heat stress transcriptional memory in Arabidopsis seedling

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Heat acclimation memory: Does the de-acclimated transcriptome reveal epigenetic processes of transcriptional regulation?

Project description:Heat acclimation (AC) allows its faster re-induction following its decline. Constitutively preserved euchromatin state in hsp70 promoter during acclimation decline/regain pushed forward the hypothesis that acclimation decline is a period of M-bM-^@M-^\dormant memoryM-bM-^@M-^] involving molecular program including epigenetic controlled transcriptional regulation leading to heat acclimation mediated cytoprotective memory. We used microarray to uncover hallmark pathways in the induction of heat-acclimation-mediated memory, focusing on markers of epigenetic processes. Rats subjected to heat acclimation, deacclimation, reacclimation and untreated controls were used. We showed here that (i) AC2d provides the molecular switch for acclimation (ii) AC30 heart demonstrates qualitative adaptations (iii) specific molecular program encompassing up/down regulated gene during DeAC, of which epigenetic markers such as class A histones, chromatin modifiers and microRNA suggest epigenetic transcriptional regulation linked to acclimation memory (iv) constitutive upregulation of MAPK P38 module and targets as well as jak/stat and AKT associated pathways during DeAC imply its major role in this process. Noteworthy are players such as poly-(ADP-ribose)polymerase-1 (PARP1) and linker histones (histones H1 cluster in this process).

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