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Histone deacetylase HDA710 controls salt tolerance by regulating ABA signaling in rice
Author(s) -
Ullah Farhan,
Xu Qiutao,
Zhao Yu,
Zhou DaoXiu
Publication year - 2021
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.13042
Subject(s) - abscisic acid , acetylation , histone deacetylase , histone , jasmonic acid , biology , genetically modified rice , microbiology and biotechnology , histone h4 , mutant , abiotic stress , oryza sativa , wild type , gene , transgene , genetics , genetically modified crops
Plants have evolved numerous mechanisms that assist them in withstanding environmental stresses. Histone deacetylases (HDACs) play crucial roles in plant stress responses; however, their regulatory mechanisms remain poorly understood. Here, we explored the function of HDA710/OsHDAC2, a member of the HDAC RPD3/HDA1 family, in stress tolerance in rice ( Oryza sativa ). We established that HDA710 localizes to both the nucleus and cytoplasm and is involved in regulating the acetylation of histone H3 and H4, specifically targeting H4K5 and H4K16 under normal conditions. HDA710 transcript accumulation levels were strongly induced by abiotic stresses including drought and salinity, as well as by the phytohormones jasmonic acid (JA) and abscisic acid (ABA). hda710 knockout mutant plants showed enhanced salinity tolerance and reduced ABA sensitivity, whereas transgenic plants overexpressing HDA710 displayed the opposite phenotypes. Moreover, ABA‐ and salt‐stress‐responsive genes, such as OsLEA3, OsABI5, OsbZIP72 , and OsNHX1 , were upregulated in hda710 compared with wild‐type plants. These expression differences corresponded with higher levels of histone H4 acetylation in gene promoter regions in hda710 compared with the wild type under ABA and salt‐stress treatment. Collectively, these results suggest that HDA710 is involved in regulating ABA‐ and salt‐stress‐responsive genes by altering H4 acetylation levels in their promoters.