TOR represses stress responses through global regulation of H3K27 trimethylation in plants.
Yihan DongVeli V UsluAlexandre BerrGaurav SinghCsaba PapdiVictor A SteffensThierry HeitzLyubov A RyabovaPublished in: Journal of experimental botany (2022)
Target of Rapamycin (TOR) functions as a central sensory hub to link a wide range of external stimuli to gene expression. However, the mechanisms underlying stimulus-specific transcriptional reprogramming by TOR remain elusive. Our in silico analysis in Arabidopsis demonstrates that TOR-repressed genes are associated with either bistable or silent chromatin states. Both states regulated by the TOR signaling pathway are associated with a high level of histone H3K27 trimethylation (H3K27me3) deposited by CURLY LEAF (CLF) in a specific context with LIKE HETEROCHROMATIN PROTEIN1 (LHP1). The combination of the two epigenetic histone modifications, H3K4me3 and H3K27me3, implicates a bistable feature which alternates between on and off state allowing rapid transcriptional changes upon external stimuli. Chromatin remodeler SWI2/SNF2 ATPase BRAHMA (BRM) activates TOR-repressed genes only at bistable chromatin domains to rapidly induce biotic stress responses. Here, we demonstrated both in silico and in vivo that TOR represses transcriptional stress responses through global maintenance of H3K27me3.
Keyphrases
- gene expression
- transcription factor
- dna methylation
- genome wide
- dna damage
- signaling pathway
- molecular docking
- bioinformatics analysis
- genome wide identification
- oxidative stress
- deep learning
- cell proliferation
- pi k akt
- network analysis
- heat shock
- loop mediated isothermal amplification
- molecular dynamics simulations