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首页> 外文期刊>Plant and cell physiology >Ky-2, a Histone Deacetylase Inhibitor, Enhances High-Salinity Stress Tolerance in Arabidopsis thaliana
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Ky-2, a Histone Deacetylase Inhibitor, Enhances High-Salinity Stress Tolerance in Arabidopsis thaliana

机译:Ky-2,组蛋白脱乙酰基酶抑制剂,提高拟南芥的高盐度胁迫耐受性

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Adaptation to environmental stress requires genome-wide changes in gene expression. Histone modifications are involved in gene regulation, but the role of histone modifications under environmental stress is not well understood. To reveal the relationship between histone modification and environmental stress, we assessed the effects of inhibitors of histone modification enzymes during salinity stress. Treatment with Ky-2, a histone deacetylase inhibitor, enhanced high-salinity stress tolerance in Arabidopsis. We confirmed that Ky-2 possessed inhibition activity towards histone deacetylases by immunoblot analysis. To investigate how Ky-2 improved salt stress tolerance, we performed transcriptome and metabolome analysis. These data showed that the expression of salt-responsive genes and salt stress-related metabolites were increased by Ky-2 treatment under salinity stress. A mutant deficient in AtSOS1 (Arabidopis thaliana SALT OVERLY SENSITIVE 1), which encodes an Na+/H+ antiporter and was among the up-regulated genes, lost the salinity stress tolerance conferred by Ky-2. We confirmed that acetylation of histone H4 at AtSOS1 was increased by Ky-2 treatment. Moreover, Ky-2 treatment decreased the intracellular Na+ accumulation under salinity stress, suggesting that enhancement of SOS1-dependent Na+ efflux contributes to increased high-salinity stress tolerance caused by Ky-2 treatment.
机译:适应环境压力需要基因表达范围内的全基因组变化。组蛋白修饰参与基因调控,但对组蛋白修饰在环境压力下的作用尚不十分了解。为了揭示组蛋白修饰与环境胁迫之间的关系,我们评估了盐分胁迫期间组蛋白修饰酶抑制剂的作用。组蛋白脱乙酰基酶抑制剂Ky-2的处理增强了拟南芥的高盐度胁迫耐受性。我们通过免疫印迹分析证实Ky-2对组蛋白脱乙酰基酶具有抑制活性。为了研究Ky-2如何改善盐胁迫耐受性,我们进行了转录组和代谢组分析。这些数据表明在盐胁迫下,通过Ky-2处理,盐反应基因和盐胁迫相关代谢产物的表达增加。一个缺少AtSOS1的突变体(拟南拟南芥SALT过度敏感1),其编码Na + / H +反转运蛋白,并且是上调基因之一,但失去了Ky-2赋予的盐胁迫耐受性。我们证实,通过Ky-2处理,AtSOS1处的组蛋白H4的乙酰化作用增加。此外,Ky-2处理降低了盐分胁迫下细胞内Na +的积累,表明SOS1依赖性Na +外排的增强有助于增加由Ky-2处理引起的高盐分胁迫耐受性。

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