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一种新型的富含甘氨酸的结构域蛋白 GRDP1,作为一个关键的反馈调节因子,在控制水稻细胞死亡和抗病性方面发挥作用。

A novel glycine-rich domain protein, GRDP1, functions as a critical feedback regulator for controlling cell death and disease resistance in rice.

机构信息

State Key Laboratory of Agrobiotechnology and College of Plant Protection, China Agricultural University, Beijing, China.

出版信息

J Exp Bot. 2021 Feb 2;72(2):608-622. doi: 10.1093/jxb/eraa450.

DOI:10.1093/jxb/eraa450
PMID:32995857
Abstract

Lesion mimic mutants constitute a valuable genetic resource for unraveling the signaling pathways and molecular mechanisms governing the programmed cell death and defense responses of plants. Here, we identified a lesion mimic mutant, spl-D, from T-DNA insertion rice lines. The mutant exhibited higher accumulation of H2O2, spontaneous cell death, decreased chlorophyll content, up-regulation of defense-related genes, and enhanced disease resistance. The causative gene, OsGRDP1, encodes a cytosol- and membrane-associated glycine-rich domain protein. OsGRDP1 was expressed constitutively in all of the organs of the wild-type plant, but was up-regulated throughout plant development in the spl-D mutant. Both the overexpression and knockdown (RNAi) of OsGRDP1 resulted in the lesion mimic phenotype. Moreover, the intact-protein level of OsGRDP1 was reduced in the spotted leaves from both overexpression and RNAi plants, suggesting that the disruption of intact OsGRDP1 is responsible for lesion formation. OsGRDP1 interacted with an aspartic proteinase, OsAP25. In the spl-D and overexpression plants, proteinase activity was elevated, and lesion formation was partially suppressed by an aspartic proteinase inhibitor. Taken together, our results reveal that OsGRDP1 is a critical feedback regulator, thus contributing to the elucidation of the mechanism underlying cell death and disease resistance.

摘要

病变模拟突变体是解析植物程序性细胞死亡和防御反应信号通路和分子机制的宝贵遗传资源。在这里,我们从 T-DNA 插入水稻品系中鉴定出一个病变模拟突变体 spl-D。该突变体表现出更高的 H2O2 积累、自发细胞死亡、叶绿素含量降低、防御相关基因上调和增强的抗病性。致病基因 OsGRDP1 编码一种细胞质和膜相关的甘氨酸丰富结构域蛋白。OsGRDP1 在野生型植物的所有器官中持续表达,但在 spl-D 突变体中整个发育过程中均上调表达。OsGRDP1 的过表达和敲低(RNAi)都导致了病变模拟表型。此外,过表达和 RNAi 植株的斑点叶片中完整蛋白水平的 OsGRDP1 降低,表明完整 OsGRDP1 的破坏是导致病变形成的原因。OsGRDP1 与天冬氨酸蛋白酶 OsAP25 相互作用。在 spl-D 和过表达植株中,蛋白酶活性升高,天冬氨酸蛋白酶抑制剂部分抑制了病变的形成。综上所述,我们的结果表明 OsGRDP1 是一个关键的反馈调节因子,有助于阐明细胞死亡和抗病性的机制。

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