H3K4me3
细胞生物学
组蛋白
脱甲基酶
突变体
非生物胁迫
转录因子
化学
串扰
表观遗传学
渗透压
生物化学
组蛋白脱乙酰基酶2
去甲基化
盐度
生物
组蛋白脱乙酰基酶
抄写(语言学)
水稻
非生物成分
基因沉默
拟南芥
酶
组蛋白甲基化
光敏色素
组蛋白H3
过氧化物酶
转录调控
作者
Jing Wang,Zhengting Chen,Pengxiang Bai,B Liu,Lingling Meng,Jian Zhang,Li X,Dao‐Xiu Zhou,Xuan Ma,Yu Zhao
摘要
Soil salinity poses a significant threat to global crop productivity. Understanding the molecular mechanisms underlying plant response to salt stress is crucial for enhancing crop resilience and yield. Here, we show that histone demethylase JMJ704 interacts with HDA709, a deacetylase that is specific for H3K9ac, to synergistically modulate salt tolerance in rice. Genetic analysis revealed that overexpressing either JMJ704 or HDA709 enhanced salt sensitivity, whereas the hda709 mutant exhibited a salt-tolerant phenotype. Interestingly, while the jmj704 mutant showed no significant change in salt sensitivity, the jmj704hda709 double mutant demonstrated markedly improved salt tolerance. Immunoblot analysis showed bidirectional crosstalk between JMJ704-catalyzed H3K4me3 demethylation and HDA709-mediated H3K9ac deacetylation, with both enzymes exhibiting synergistic functional interplay. We further demonstrated that under salt stress, JMJ704 forms a chromatin-modifying complex with HDA709, which, together with the transcription factor OsWRKY72, co-regulates peroxidase and salt-responsive genes. This recruitment facilitates transcriptional silencing through concurrent erasure of H3K4me3 and H3K9ac marks. Collectively, our work reveals that the JMJ704-HDA709 complex interacts with OsWRKY72 to negatively regulate rice salt tolerance by modulating ROS metabolism and salt-responsive genes. This finding provides evidence for the pivotal role of epigenetic regulation of plant abiotic stress responses and offers new insights for developing stress-resilient crops.
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