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组蛋白乙酰转移酶 GCN5 通过改变纤维素合成基因的表达来促进细胞壁完整性和耐盐胁迫。

Histone acetyltransferase GCN5 contributes to cell wall integrity and salt stress tolerance by altering the expression of cellulose synthesis genes.

机构信息

State Key Laboratory for Agrobiotechnology and Key Laboratory of Crop Heterosis and Utilization (MOE) and Beijing Key Laboratory of Crop Genetic Improvement, Joint Laboratory for International Cooperation in Crop Molecular Breeding, Ministry of Education, China Agricultural University, Beijing, 100193, China.

Institute of Plant Science Paris-Saclay, Université Paris Sud, 91405, Orsay, France.

出版信息

Plant J. 2019 Feb;97(3):587-602. doi: 10.1111/tpj.14144. Epub 2018 Dec 12.

DOI:10.1111/tpj.14144
PMID:30394596
Abstract

Excess soluble salts in soil are harmful to the growth and development of most plants. Evidence is emerging that the plant cell wall is involved in sensing and responding to salt stress, but the underlying mechanisms are not well understood. We reveal that the histone acetyltransferase General control non-repressed protein 5 (GCN5) is required for the maintenance of cell wall integrity and salt stress tolerance. The levels of GCN5 mRNA are increased in response to salt stress. The gcn5 mutants exhibited severe growth inhibition and defects in cell wall integrity under salt stress conditions. Combining RNA sequencing and chromatin immunoprecipitation assays, we identified the chitinase-like gene CTL1, polygalacturonase involved in expansion-3 (PGX3) and MYB domain protein-54 (MYB54) as direct targets of GCN5. Acetylation of H3K9 and H3K14 mediated by GCN5 is associated with activation of CTL1, PGX3 and MYB54 under salt stress. Moreover, constitutive expression of CTL1 in the gcn5 mutant restores salt tolerance and cell wall integrity. In addition, the expression of the wheat TaGCN5 gene in Arabidopsis gcn5 mutant plants complemented the salt tolerance and cell wall integrity phenotypes, suggesting that GCN5-mediated salt tolerance is conserved between Arabidopsis and wheat. Taken together, our data indicate that GCN5 plays a key role in the preservation of salt tolerance via versatile regulation in plants.

摘要

土壤中过量的可溶性盐对大多数植物的生长和发育有害。有证据表明,植物细胞壁参与了对盐胁迫的感知和响应,但潜在的机制尚不清楚。我们揭示了组蛋白乙酰转移酶一般控制非阻遏蛋白 5(GCN5)是维持细胞壁完整性和耐盐胁迫所必需的。GCN5 mRNA 的水平会因盐胁迫而增加。gcn5 突变体在盐胁迫条件下表现出严重的生长抑制和细胞壁完整性缺陷。通过 RNA 测序和染色质免疫沉淀分析,我们鉴定了几丁质酶样基因 CTL1、参与扩张的多聚半乳糖醛酸酶 3(PGX3)和 MYB 结构域蛋白 54(MYB54)是 GCN5 的直接靶标。GCN5 介导的 H3K9 和 H3K14 的乙酰化与 CTL1、PGX3 和 MYB54 在盐胁迫下的激活有关。此外,在 gcn5 突变体中组成性表达 CTL1 可恢复耐盐性和细胞壁完整性。此外,在拟南芥 gcn5 突变体植物中表达小麦 TaGCN5 基因补充了耐盐性和细胞壁完整性表型,这表明 GCN5 介导的耐盐性在拟南芥和小麦之间是保守的。总之,我们的数据表明,GCN5 通过在植物中的多种调节作用,在保持耐盐性方面发挥着关键作用。

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