OsHDAC1 deacetylates the aldehyde dehydrogenase OsALDH2B1, repressing OsGR3 and decreasing salt tolerance in rice

Abstract

Salt stress poses a significant challenge to the growth and productivity of rice (Oryza sativa L.). Histone deacetylases (HDACs) play a vital role in modulating responses to various abiotic stresses. However, how OsHDAC1 responds to salt stress remains largely unknown. Here, we report that OsHDAC1 decreases salt tolerance in rice through post-translational modification of metabolic enzymes. Specifically, the rice OsHDAC1 RNAi lines exhibited enhanced resilience to salt stress, while plants overexpressing OsHDAC1 were notably more sensitive. OsHDAC1 interacts with the aldehyde dehydrogenase (ALDH) OsALDH2B1 and deacetylates it at K311 and K531, triggering ubiquitin-proteasome-mediated degradation of OsALDH2B1. OsALDH2B1 can directly target OsGR3, which encodes a type of glutathione reductase critical for reactive oxygen species (ROS) scavenging. Compared with wild-type plants, OsALDH2B1-overexpressing plants exhibited higher OsGR3 expression levels and increased salt resistance, whereas OsALDH2B1 RNAi lines showed reduced OsGR3 expression and lower salt resistance. Collectively, our data suggest that salt stress down-regulates OsHDAC1, resulting in an increase in the acetylation level of OsALDH2B1, which in turn stabilizes OsALDH2B1 and promotes its activity in the regulation of OsGR3 transcription. This OsHDAC1/OsALDH2B1/OsGR3 regulatory module represents an alternative pathway for governing salt stress adaptation in rice.

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