Histone deacetylase OsHDA716 chilling out with OsbZIP46: antagonistically regulating cold stress tolerance in rice

Abstract

Plants do not have the luxury of having heated rooms during cold winters as we do.Therefore, to enhance plant cold tolerance and boost agricultural productivity, it is imperative to fully understand how cold perception is signalled inside the cells to activate mechanisms that protect plants from cold damage.It is well studied that a transcriptional cascade involving C-REPEAT BINDING FACTOR/DEHYDRATION-RESPONSIVE ELEMENT-BINDING PROTEIN 1 (CBF/DREB1) induces rapid changes in intracellular calcium levels upon cold stress (Yuan et al. 2018).However, epigenetic mechanisms involved in cold signal transduction are largely unknown, even though epigenetic regulation of gene expression has an essential role in plant adaptation to various environmental changes.Indeed, previous studies demonstrated that histone acetylation/deacetylation is essential to control gene expression in response to abiotic stress (Cheng et al. 2018).Histone deacetylases (HDACs) cause chromatin compaction through the deacetylation of lysine residues in histones, thereby reducing the accessibility of the transcription machinery to gene promoters (Zheng et al. 2020).However, their potential histone-independent functions in cold stress responses remain unexplored.In this issue of The Plant Cell, Ying Sun and colleagues (Sun et al. 2023) provide a thorough analysis of how the histone deacetylase OsHDA716 mediates fine-tuning of cold responses in rice by a histone-independent mechanism.Through gene expression analysis in cold conditions, the authors identified OsHDA716 as a highly responsive gene to cold temperatures.Functional characterization of rice plants with either loss or overexpression of OsHDA716 showed that it is a negative regulator of cold stress tolerance because loss-of-function mutants were more resistant to cold, whereas plants overexpressing the deacetylase were more susceptible.The authors then turned to analyze the implication of calcium in this process.They used Scanning Ion-selective Electrode Technique (SIET) and Fluo-4 acetoxymethyl ester as fluorescent indicators of [Ca 2+ ] cyt and observed the impact of OsHDA716 on cold-induced Ca 2+ influx.The results indicated that the negative regulation of rice chilling tolerance by OsHDA716 is connected to a compromised elevation of Ca 2+ upon cold induction.Sun et al. further teased out the molecular mechanism underlying this regulatory process by the identification of the transcription factor OsbZIP46 as a protein interaction partner of OsHDA716 using yeast two-hybrid screening.Protein-protein interaction studies confirmed that OsHDA716 physically interacts with OsbZIP46 in vitro and in vivo.Importantly, the expression of OsbZIP46 increases during chilling stress.

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