Explore the vast range of titles available.

Pre-exposing (priming) plants to mild, non-lethal elevated temperature improves their tolerance to a later higher-temperature stress (triggering stimulus), which is of great ecological importance. ‘Thermomemory’ is maintaining this tolerance for an extended period of time. NAM/ATAF1/2/CUC2 (NAC) proteins are plant-specific transcription factors (TFs) that modulate responses to abiotic stresses, including heat stress (HS). Here, we investigated the potential role of NACs for thermomemory. We determined the expression of 104 Arabidopsis NAC genes after priming and triggering heat stimuli, and found ATAF1 expression is strongly induced right after priming and declines below control levels thereafter during thermorecovery. Knockout mutants of ATAF1 show better thermomemory than wild type, revealing a negative regulatory role. Differential expression analyses of RNA-seq data from ATAF1 overexpressor, ataf1 mutant and wild-type plants after heat priming revealed five genes that might be priming-associated direct targets of ATAF1: AT2G31260 ( ATG9 ), AT2G41640 ( GT61 ), AT3G44990 ( XTH31 ), AT4G27720 and AT3G23540 . Based on co-expression analyses applied to the aforementioned RNA-seq profiles, we identified ANAC055 to be transcriptionally co-regulated with ATAF1 . Like ataf1 , anac055 mutants show improved thermomemory, revealing a potential co-control of both NAC TFs over thermomemory. Our data reveals a core importance of two NAC transcription factors, ATAF1 and ANAC055, for thermomemory.

Long-term salinity stress induces senescence, probably through an involvement of hydrogen peroxide (H2O2)-mediated signalling. This study identifies candidate H2O2-responsive cis-regulatory elements governing gene expression during salinity stress-triggered and developmental senescence.

The transition from juvenility through maturation to senescence is a complex process that involves the regulation of longevity. Here, we identify JUNGBRUNNEN1 (JUB1), a hydrogen peroxide (H₂O₂)-induced NAC transcription factor, as a central longevity regulator in Arabidopsis thaliana. JUB1 overexpression strongly delays senescence, dampens intracellular H₂O₂ levels, and enhances tolerance to various abiotic stresses, whereas in jub1-1 knockdown plants, precocious senescence and lowered abiotic stress tolerance are observed. A JUB1 binding site containing a RRYGCCGT core sequence is present in the promoter of DREB2A, which plays an important role in abiotic stress responses. JUB1 transactivates DREB2A expression in mesophyll cell protoplasts and transgenic plants and binds directly to the DREB2A promoter. Transcriptome profiling of JUB1 overexpressors revealed elevated expression of several reactive oxygen species-responsive genes, including heat shock protein and glutathione S-transferase genes, whose expression is further induced by H₂O₂ treatment. Metabolite profiling identified elevated Pro and trehalose levels in JUB1 overexpressors, in accordance with their enhanced abiotic stress tolerance. We suggest that JUB1 constitutes a central regulator of a finely tuned control system that modulates cellular H₂O₂ level and primes the plants for upcoming stress through a gene regulatory network that involves DREB2A.

Rapid climate change demands the development of heat-resilient plants. Elevated temperatures perturb cellular protein homeostasis, and its timely restoration is crucial for plant survival after stress. Thermopriming, which involves pre-exposure to sublethal heat stress, has emerged as a promising strategy for enhancing heat stress tolerance. However, the impact of thermopriming on protein homeostasis remains unclear. Here, we demonstrate that priming-mediated acquired thermotolerance involves the dynamic regulation of protein maintenance and clearance mechanisms. Priming facilitates the activation of heat shock response (HSR) via HSFA1, and unfolded protein response (UPR). Simultaneously, priming induces the protein clearance pathway, namely autophagy, potentially through the dynamic modulation of autophagy-negative regulators. Contrastingly, unprimed seedlings fail to mount HSR and UPR, resulting in disrupted proteostasis and the accumulation of aggregates, and ultimately fail to survive. While the loss of UPR was found to have a minimal impact on priming-mediated outcomes, the HSR response proved essential, as its absence led to lethality under heat stress. Additionally, the absence of HSR was found to enhance the autophagy response post-stress. Our results highlight the critical role of protein maintenance mechanisms over clearance pathways in ensuring survival. Taken together, our study demonstrates that thermopriming enhances heat stress resilience by temporally coordinating autophagy, HSR and UPR responses to maintain proteostasis.

Rice, a staple cereal crop, faces significant threats from rising temperatures, affecting all growth stages including early seedling establishment. Despite being critical in determining overall growth and productivity, response to heat stress during the early seedling stage remains understudied. This research aimed to assess the impact of acute heat stress on rice seedlings and unravel underlying molecular mechanisms. Rice seedlings were exposed to varying intensities and durations of heat stress to determine a critical threshold affecting growth. To elucidate the transcription factor (TF)-mediated regulatory mechanisms and their functional interactome in response to stress, transcriptomic analysis of shoots and roots exposed to acute heat stress was performed. Transcriptome analysis unveiled a comprehensive TF-target regulatory map for shoots and roots, potentially involved in the modulation of growth-defence trade-off in response to acute heat stress. Ethylene Responsive Factors (ERFs) emerged as central regulators, with phytohormones ethylene and jasmonic acid acting as upstream modulators. Pre-treatment with these phytohormones alleviated the adverse effects of heat stress. This study uncovers key molecular mechanisms governing rice seedling responses to acute heat stress involving ERFs-hormonal interactions. Modulating these core regulators presents a promising strategy to enhance heat resilience, addressing global food security amid rising temperatures.