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Histone methyltransferases SDG25/ATX1 regulate heat stress memory by antagonizing DNA remethylation

ABSTRACT: Histone methyltransferases SDG25/ATX1 regulate heat stress memory by antagonizing DNA remethylation

PROVIDER: PRJNA641644 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12082109_1.fastq.gz	Fastqsanger.gz
	SRR12082109_2.fastq.gz	Fastqsanger.gz
	SRR12082110_1.fastq.gz	Fastqsanger.gz
	SRR12082110_2.fastq.gz	Fastqsanger.gz
	SRR12082111_1.fastq.gz	Fastqsanger.gz

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Histone methyltransferases SDG25/ATX1 regulate heat stress memory by antagonizing DNA remethylation

Project description:Heat stress is a great threat to plant growth because of their sessile lifestyle. Here, we show that histone methyltransferases SDG25 and ATX1 regulate gene expression and antagonize DNA remethylation under recovery stage after long-term high temperature treatment by catalyzing the methylation of histone H3K4 loci.

2021-06-24 | GSE153159 | GEO

Transcriptomic analysis of heat stress transcriptional memory in Arabidopsis seedling

Project description:Plants can be primed by a stress cue to mount a faster and stronger activation of defense mechanisms upon a subsequent stress. A crucial component of such stress priming is the modified reactivation of genes upon recurring stress, a phenomenon known as transcriptional memory. The transcriptional memory in response to heat stress is not clear at the genome scale. We used microarrays to identify genes that showed transcriptional memory in response to recurring heat stress.

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

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Heat-induced transgenerational memory of upregulated gene expression

Project description:Heat-induced transgenerational memory of upregulated gene expression

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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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Heteromeric HSFA2/HSFA3 complexes drive transcriptional memory after heat stress in Arabidopsis

Project description:Adaptive plasticity in stress responses is a key element of plant survival strategies. For instance, moderate heat stress (HS) primes a plant to acquire thermotolerance, which allows subsequent survival of more severe HS conditions. Acquired thermotolerance is actively maintained over several days (HS memory) and involves the sustained induction of memory-related genes. We find FORGETTER3/ HEAT SHOCK TRANSCRIPTION FACTOR A3 (FGT3/HSFA3) to be specifically required for physiological HS memory and maintaining high memory-gene expression during the days following a HS exposure. HSFA3 mediates HS memory by direct transcriptional activation of memory-related genes after return to normal growth temperatures. HSFA3 binds HSFA2, and in vivo both proteins form heteromeric complexes with additional HSFs. Our results indicate that only complexes containing both HSFA2 and HSFA3 efficiently promote transcriptional memory by promoting histone H3 lysine 4 (H3K4) hyper-methylation. In summary, our work defines the major HSF complex controlling transcriptional memory and elucidates the in vivo dynamics of HSF complexes during somatic stress memory.

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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.

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BRU1 is required for Heat Stress Memory in Arabidopsis

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Comparative characterization of the seven H3K4 methyltransferases in Arabidopsis thaliana

Project description:Methylation of H3 lysine 4 (H3K4me) marks transcribed elements of eukaryotic genome, and their distribution alters dynamically through developmental stages and environmental change. These dynamic regulations are likely achieved by combinatorial work of H3K4me writers, which multi-cellular organisms carry multiple copies of. To better understand the chromatin targeting mechanisms of H3K4 methyltransferase in plants, here we comparatively characterized the seven H3K4 methyltransferases in model plants Arabidopsis. This work clarified, in combination with previous results, ATX1-5 (TRX/TRR-type methyltransferase) localizes on loci with specific sets of chromatin modifications and DNA motifs. Notably, ATX3 localizes to binding motifs of ASR3 and RAP2.11 transcriptional factors and also directly interacts with those TFs. ATXR7(SET1-type) and ATXR3 (non-canonical H3K4 methyltransferase) seemed co-transcriptional. Interestingly, ATXR3, the major H3K4me3 methyltransferase in Arabidopsis, was not associated with COMPASS, which suggests H3K4me3 regulation in plants and animals is divergent. Our work provides a foundation for understanding the regulation of H3K4 methyltransferases in plants.

2024-09-23 | GSE277439 | GEO

Selective autophagy regulates heat stress memory by NBR1-mediated targeting of HSP90 and ROF1

Project description:In nature, plants are constantly exposed to many transient, but recurring, stresses. Thus, to complete their life cycles they require a dynamic balance between capacities to recover following cessation of stress and maintenance of stress memory. Recently, we uncovered a new functional role of autophagy in regulating recovery from heat stress (HS) and resetting cellular memory of HS in Arabidopsis thaliana. Here, we demonstrate that NBR1 (Next-to-BRCA1) plays a crucial role as an adaptor receptor for selective autophagy during recovery from HS. Immunoblot analysis and confocal microscopy revealed that levels of NBR1 protein, NBR1-labeled puncta and NBR1 activities were all higher during the HS recovery phase than before and after this phase. Co-immunoprecipitation analysis of proteins interacting with NBR1 and comparative proteomic analysis of a nbr1 knockout mutant and wild-type plants identified 58 proteins as potential novel targets of NBR1. Cellular, biochemical and functional genetic studies confirmed that NBR1 targets Heat Shock Protein 90 (HSP90) and ROF1, a member of the FKBP family, and mediates their degradation by autophagy, which represses the expression of HSPs regulated by HsfA2 transcription factor and the response to HS. Accordingly, loss-of-function mutation of NBR1 resulted in a stronger HS memory phenotype. Together our results provide new insights into the mechanistic principles by which autophagy regulates plant response to recurrent HS.

2022-02-15 | PXD015027 | Pride

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