RESUMEN

Among the rich repertoire of strategies that allow plants to adapt to high-temperature stress is heat-stress memory. The mechanisms underlying the establishment and maintenance of heat-stress memory are poorly understood, although the chromatin opening state appears to be an important structural basis for maintaining heat-stress memory. The chromatin opening state is influenced by epigenetic modifications, making DNA and histone modifications important entry points for understanding heat-shock memory. Current research suggests that traditional heat-stress signaling pathway components might be involved in chromatin opening, thereby promoting the establishment of heat-stress memory in plants. In this review, we discuss the relationship between chromatin structure-based maintenance and the establishment of heat-stress memory. We also discuss the association between traditional heat-stress signals and epigenetic modifications. Finally, we discuss potential research ideas for exploring plant adaptation to high-temperature stress in the future.

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RESUMEN

Heat stress limits plant growth, development, and crop yield, but how plant cells precisely sense and transduce heat stress signals remains elusive. Here, we identified a conserved heat stress response mechanism to elucidate how heat stress signal is transmitted from the cytoplasm into the nucleus for epigenetic modifiers. We demonstrate that HISTONE DEACETYLASE 9 (HDA9) transduces heat signals from the cytoplasm to the nucleus to play a positive regulatory role in heat responses in Arabidopsis. Heat specifically induces HDA9 accumulation in the nucleus. Under heat stress, the phosphatase PP2AB'ß directly interacts with and dephosphorylates HDA9 to protect HDA9 from 26S proteasome-mediated degradation, leading to the translocation of nonphosphorylated HDA9 to the nucleus. This heat-induced enrichment of HDA9 in the nucleus depends on the nucleoporin HOS1. In the nucleus, HDA9 binds and deacetylates the target genes related to signaling transduction and plant development to repress gene expression in a transcription factor YIN YANG 1-dependent and -independent manner, resulting in rebalance of plant development and heat response. Therefore, we uncover an HDA9-mediated positive regulatory module in the heat shock signal transduction pathway. More important, this cytoplasm-to-nucleus translocation of HDA9 in response to heat stress is conserved in wheat and rice, which confers the mechanism significant implication potential for crop breeding to cope with global climate warming.

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Brassinosteroids (BRs) are essential plant growth- and development-regulating phytohormones. When applied exogenously, BRs ameliorate heat shock (HS)-induced cell damage and enhance plant thermotolerance; however, the molecular mechanism by which BRs regulate plant thermotolerance is unknown. In this study, by analyzing the thermotolerance of a series of BR signaling mutants and plants that overexpressed different BR signaling components, we obtained comprehensive data showing that BRASSINOSTEROID INSENSITIVE 2 (BIN2) plays a major role in mediating the crosstalk between BR signaling and plant HS responses. By RNA-Seq, 608 HS- and BIN2-regulated genes were identified. An analysis of the 1-kb promoter sequences of these genes showed enrichment of an abscisic acid (ABA) INSENSITIVE 5 (ABI5)-binding cis-element. Physiological studies showed that thermotolerance was reduced in bin2-1 mutant and ABI5-OX plants but increased in the abi5 mutant, and that the abi5 mutation could recover the thermotolerance of bin2-1 plants to a wild-type level, suggesting that ABI5 functions downstream of BIN2 in regulating plant thermotolerance. Further, HS treatment increased the cellular abundance of BIN2. Both bin2-1 mutant and BIN2-OX plants showed early flowering, while the BIN2 loss-of-function mutant bin2-3 bil1 bil2 flowered late. Given these findings, we propose that under HS conditions plants increase BIN2 activity to promote early flowering and ensure species survival; however, this reduces the thermotolerance and survivability of individual plants partially by activating ABI5.