Improved pathogen and stress tolerance in tomato mutants of SET domain histone 3 lysine methyltransferases

Improved pathogen and stress tolerance in tomato mutants of SET domain histone 3 lysine methyltransferases
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DOI:
10.1111/nph.18277
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发表时间:
2022-06-17
期刊:
影响因子:
9.4
通讯作者:
Mengiste, Tesfaye
Mengiste, Tesfaye
中科院分区:
生物学1区
文献类型:
--
作者:
Bvindi, Carol;Lee, Sanghun;Mengiste, Tesfaye

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组蛋白赖氨酸甲基化(HLMs)与不同真核生物的基因表达调控有关。然而,HLMS在调节理想的作物性状中的作用以及这些修饰所涉及的酶还知之甚少。我们研究了番茄组蛋白H3赖氨酸甲基转移酶SET结构域33(SDG33)和SDG34在生物和非生物胁迫反应中的功能。SDG33和SDG34基因编辑的突变体在H3K36和H3K4的甲基化以及参与不同过程和对生物和非生物刺激的反应的基因的表达发生了变化。两个突变体而不是单一突变体表现出对真菌病原菌灰霉病菌的抗性。有趣的是,单突变体表现出较强的耐旱性,而双突变体表现出较强的耐旱性和与独立和加性作用相一致的植株生长。突变体在干旱期间保持了较高的水分状况,并在干旱过去后改善了恢复和存活。值得注意的是,在受到攻击的植物中,H3K4和H3K36三甲基化的减少和负调控因子的表达有助于突变体的逆境耐受性。SDG33和SDG34的突变可能通过破坏允许的转录环境促进负调控因子的表达来消除生物和非生物应激的易感性。这使得可以通过修改组蛋白表观遗传标记来提高胁迫和病原体的耐受性,而不需要对生长进行权衡。
Histone lysine methylations (HLMs) are implicated in control of gene expression in different eukaryotes. However, the role of HLMs in regulating desirable crop traits and the enzymes involved in these modifications are poorly understood. We studied the functions of tomato histone H3 lysine methyltransferases SET Domain Group 33 (SDG33) and SDG34 in biotic and abiotic stress responses. SDG33 and SDG34 gene edited mutants were altered in H3K36 and H3K4 methylations, and expression of genes involved in diverse processes and responses to biotic and abiotic stimuli. The double but not the single mutants show resistance to the fungal pathogen Botrytis cinerea. Interestingly, single mutants were tolerant to drought and the double mutant showed superior tolerance and plant growth consistent with independent and additive functions. Mutants maintained higher water status during drought and improved recovery and survival after lapse of drought. Notably, diminution of H3K4 and H3K36 trimethylation and expression of negative regulators in challenged plants contributes to stress tolerance of the mutants. Mutations in SDG33 and SDG34 are likely to remove predisposition to biotic and abiotic stress by disrupting permissive transcriptional context promoting expression of negative regulatory factors. These allows improvement of stress and pathogen tolerance, without growth trade-offs, through modification of histone epigenetic marks.