TOR coordinates with transcriptional and chromatin machinery to regulate thermotolerance and thermomemory

Global warming exhibits profound effects on plant fitness and productivity. To withstand stress, plants sacrifice their growth and activate protective stress responses for ensuring survival. However, the switch between growth and stress is largely elusive. In the past decade, emerging role of Target of Rapamycin (TOR) has been studied linking energy and stress signaling. Here, we have identified an important role of Glc-TOR signaling in plant adaptation to heat stress (HS). We show that Glc-TOR signaling regulates thermotolerance and thermomemory response through distinct mechanisms. Glc-TOR via E2Fa signaling module governs the transcriptome reprogramming of a myriad set of genes involved in HS protection and recovery. Glc also epigenetically governs the transcription of core HS signaling genes in a TOR-dependent manner. TOR acts in concert with p300/CREB HISTONE ACETYLTRANSFERASE1 (HAC1) and dictates the epigenetic landscape of HS loci to regulate thermotolerance. Arabidopsis plants defective in and exhibited reduced thermotolerance with a decrease in expression of core HS signaling genes. TOR also promotes accumulation of histone H3K4me3 marks at the promoters of thermomemory-related genes and therefore, governs thermomemory. Further, genome-wide transcriptome of Glc-TOR shows huge overlap with targets of chromatin remodeler BRAHMA, especially with genes enriched in stress, chromatin remodelling and histone/protein modifications. Collectively, our findings thus reveal a mechanistic framework in which Glc-TOR signalling through multiple modules determines the integration of stress and energy signaling to regulate thermotolerance and thermomemory.