MYB44-ENAP1/2 restricts HDT4 to regulate drought tolerance in Arabidopsis.

MYB44-ENAP1/2 restricts HDT4 to regulate drought tolerance in Arabidopsis.
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DOI:
10.1371/journal.pgen.1010473
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发表时间:
2022-11
期刊:
影响因子:
4.5
通讯作者:
--
中科院分区:
生物学2区
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组蛋白乙酰化已被证明参与应激反应。然而,组蛋白去乙酰化酶和转录因子在干旱胁迫反应中的作用机制尚不清楚。在本研究中,我们发现ENAP 1和ENAP 2是植物耐旱性的正向调节因子,并且enap 1 enap 2双突变体对干旱胁迫更敏感。ENAP 1和ENAP 2都与MYB 44相互作用,MYB 44是一种与组蛋白脱乙酰酶HDT 4相互作用的转录因子。遗传学数据表明,myb 44无效突变增强了enap 1 enap 2对干旱胁迫的敏感性。然而,HDT 4负调控植物干旱反应,hdt 4突变体抑制enap 1 enap 2 myb 44干旱敏感表型。在正常情况下,ENAP 1/2和MYB 44抵消HDT 4调节H3 K27 ac的功能。在干旱胁迫下,MYB 44的积累和HDT 4的减少导致H3 K27 ac的富集和目的基因表达的激活。总之,本研究提供了一种新的分子机制,即在正常条件下,ENAP 1、ENAP 2和MYB 44形成复合物限制HDT 4的功能;在干旱条件下,MYB 44的积累和HDT 4的减少导致H3 K27 ac的升高和干旱响应基因的表达,从而使植物耐旱。缺水已成为限制可持续作物生产的最大问题之一。揭示干旱胁迫响应的分子机制已成为国内外研究的热点之一。组蛋白修饰和转录因子已被证明在干旱胁迫反应中共同发挥作用。然而,详细的分子机制仍有待研究。在本研究中,我们发现了一种新的分子机制,即组蛋白结合蛋白ENAP 1和ENAP 2与MYB 44形成复合物,在正常情况下限制组蛋白去乙酰化酶HDT 4调节靶基因H3 K27乙酰化的功能;而在干旱条件下,MYB 44蛋白积累,HDT 4蛋白减少,导致H3 K27 ac的升高和干旱响应基因的表达,因此,植物是耐旱的。本研究为组蛋白去乙酰化酶、组蛋白结合蛋白和转录因子如何协同调控植物干旱胁迫反应提供了新的视角。
Histone acetylation has been shown to involve in stress responses. However, the detailed molecular mechanisms that how histone deacetylases and transcription factors function in drought stress response remain to be understood. In this research, we show that ENAP1 and ENAP2 are positive regulators of drought tolerance in plants, and the enap1enap2 double mutant is more sensitive to drought stress. Both ENAP1 and ENAP2 interact with MYB44, a transcription factor that interacts with histone deacetylase HDT4. Genetics data show that myb44 null mutation enhances the sensitivity of enap1enap2 to drought stress. Whereas, HDT4 negatively regulates plant drought response, the hdt4 mutant represses enap1enap2myb44 drought sensitive phenotype. In the normal condition, ENAP1/2 and MYB44 counteract the HDT4 function for the regulation of H3K27ac. Upon drought stress, the accumulation of MYB44 and reduction of HDT4 leads to the enrichment of H3K27ac and the activation of target gene expression. Overall, this research provides a novel molecular mechanism by which ENAP1, ENAP2 and MYB44 form a complex to restrict the function of HDT4 in the normal condition; under drought condition, accumulated MYB44 and reduced HDT4 lead to the elevation of H3K27ac and the expression of drought responsive genes, as a result, plants are drought tolerant. Water deficiency has become one of the greatest concerns limiting sustainable crop production. Uncovering the molecular mechanisms of drought stress response has been one of hot research topics worldwide. Histone modification and transcription factors have been shown to function in the drought stress response collectively. Yet, the detailed molecular mechanisms are still remained to study. In this research, we found a novel molecular mechanism that the histone binding protein ENAP1 and ENAP2 form a complex with MYB44 to restrict the function of histone deacetylase HDT4 from regulating H3K27 acetylation in the target genes in a normal condition; Whereas, under drought condition, MYB44 proteins are accumulated, and the HDT4 proteins are reduced, leading to elevations of H3K27ac and the expression of drought responsive genes, as a result, plants are drought tolerant. This research provides a new insight of how histone deacetylase, histone binding protein and transcription factor coordinate to regulate drought stress response in plants.
DOI: 10.1038/nmeth.1923
发表时间: 2012-03-04
期刊: NATURE METHODS
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