拟南芥
发芽
组蛋白
组蛋白脱乙酰基酶
生物
突变体
乙酰化
细胞生物学
染色质免疫沉淀
生物化学
植物
基因表达
基因
发起人
作者
Wensi Tang,Li Zhong,Qing‐qian Ding,Youjun Dou,Wei‐wei Li,Zhao‐Shi Xu,Yongbin Zhou,Jun Chen,Ming Chen,You‐Zhi Ma
摘要
Salt tolerance during seed germination is essential for seedling establishment under salt stress. Sirtuin-like proteins, NAD+ -dependent histone deacetylases, are involved in plant responses to abiotic stresses; however, the regulatory mechanism remains unknown. We elucidated the mechanism underlying AtSRT2 (a sirtuin-like protein)-mediated regulation of salt tolerance during seed germination in Arabidopsis. The AtSRT2 mutant srt2 exhibited significantly reduced seed germination percentages under salt stress; its targets were identified via chromatin immunoprecipitation coupled with ultra-high-throughput parallel DNA sequencing (ChIP-Seq) assay. Epistasis analysis was performed to identify AtSRT2-related pathways. Overexpression of SRT2.7, an AtSRT2 splice variant, rescued the salt-sensitive phenotype of mutant srt2. AtSRT2 histone deacetylation activity was important for salt tolerance during seed germination. The acetylation level of histone H4K8 locus in srt2-1 increased significantly under salt treatment. Vesicle-associated membrane protein 714 (VAMP714), a negative regulator of hydrogen peroxide (H2 O2 )-containing vesicle trafficking in cells, was identified as a target of AtSRT2. AtSRT2 regulated histone acetylation in the promoter region of VAMP714 and inhibited VAMP714 transcription under salt treatment. Seed germination percentage of double-mutant srt2-1vamp714 was close to that of single-mutant vamp714, and higher than that of single-mutant srt2 under salt stress. Hydrogen peroxide content and DNA damage increased after salt treatment in srt2 during seed germination. AtSRT2 regulates salt tolerance during seed germination through VAMP714 in Arabidopsis.
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