Abstract
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, the role of the target of rapamycin (TOR) linking energy and stress signalling is emerging. Here, we have identified an important role of Glucose (Glc)-TOR signalling in plant adaptation to heat stress (HS). Glc via TOR governs the transcriptome reprogramming of a large number of genes involved in heat stress protection. Downstream to Glc-TOR, the E2Fa signalling module regulates the transcription of heat shock factors through direct recruitment of E2Fa onto their promoter regions. Also, Glc epigenetically regulates the transcription of core HS signalling 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 TOR and HAC1 exhibited reduced thermotolerance with a decrease in the expression of core HS signalling genes. Together, our findings reveal a mechanistic framework in which Glc-TOR signalling through different modules integrates stress and energy signalling to regulate thermotolerance.
Highlights
Plants are immobile and are unable to escape the harmful conditions in the environment
Seedlings grown under high light (HL) without Glc showed more improved stress recovery than their low light (LL) without Glc counterparts
Seedlings grown under HL together with Glc showed the highest rate of stress recovery and increased thermotolerance (Figures 1A–C)
Summary
Plants are immobile and are unable to escape the harmful conditions in the environment. Rather, throughout evolution, they have evolved adaptive strategies to gauge and respond to stressful conditions for survival and reproductive success. At the time of stress, plants sacrifice their growth to activate stress machinery and ensure survival. Once the stress signal is receded, plants quickly downregulate the stress machinery and activate stress recovery and growth machinery. Global transcriptome profiling in response to sugars or mutants defective in sugar signalling (such as TOR mutants) showed alteration in stress-induced gene transcripts such as heat shock proteins (Mishra et al, 2009; Xiong et al, 2013; Gupta et al, 2015b). TOR is an evolutionarily conserved ser/thr kinase, which works in a multiprotein complex and is a central regulator of different
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