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烟草 TTG2 通过将 NPR1 隔离在核外抑制对病原体的抗性。

Tobacco TTG2 suppresses resistance to pathogens by sequestering NPR1 from the nucleus.

机构信息

State Ministry of Education Key Laboratory of Integrated Management of Crop Pests, Nanjing Agricultural University, China.

出版信息

J Cell Sci. 2012 Oct 15;125(Pt 20):4913-22. doi: 10.1242/jcs.111922. Epub 2012 Jul 13.

DOI:10.1242/jcs.111922
PMID:22797922
Abstract

TRANSPARENT TESTA GLABRA (TTG) proteins that contain the WD40 protein interaction domain are implicated in many signalling pathways in plants. The salicylic acid (SA) signalling pathway regulates the resistance of plants to pathogens through defence responses involving pathogenesis-related (PR) gene transcription, activated by the NPR1 (nonexpresser of PR genes 1) protein, which contains WD40-binding domains. We report that tobacco (Nicotiana tabacum) NtTTG2 suppresses the resistance to viral and bacterial pathogens by repressing the nuclear localisation of NPR1 and SA/NPR1-regulated defence in plants. Prevention of NtTTG2 protein production by silencing of the NtTTG2 gene resulted in the enhancement of resistance and PR gene expression, but NtTTG2 overexpression or NtTTG2 protein overproduction caused the opposite effects. Concurrent NtTTG2 and NPR1 gene silencing or NtTTG2 silencing in the absence of SA accumulation compensated for the compromised defence as a result of the NPR1 single-gene silencing or the absence of SA. However, NtTTG2 did not interact with NPR1 but was able to modulate the subcellular localisation of the NPR1 protein. In the absence of NtTTG2 production NPR1 was found predominantly in the nucleus and the PR genes were expressed. By contrast, when NtTTG2 accumulated in transgenic plants, a large proportion of NPR1 was retained in the cytoplasm and the PR genes were not expressed. These results suggest that NtTTG2 represses SA/NPR1-regulated defence by sequestering NPR1 from the nucleus and the transcriptional activation of the defence-response genes.

摘要

含有 WD40 蛋白相互作用域的透明种皮(TTG)蛋白参与植物中的许多信号通路。水杨酸(SA)信号通路通过涉及与发病相关(PR)基因转录的防御反应来调节植物对病原体的抗性,该反应由 NPR1(PR 基因无表达者 1)蛋白激活,该蛋白包含 WD40 结合域。我们报告说,烟草(Nicotiana tabacum)NtTTG2 通过抑制 NPR1 的核定位和植物中 SA/NPR1 调节的防御来抑制对病毒和细菌病原体的抗性。通过沉默 NtTTG2 基因抑制 NtTTG2 蛋白的产生导致抗性和 PR 基因表达增强,但 NtTTG2 过表达或 NtTTG2 蛋白过度产生导致相反的效果。同时沉默 NtTTG2 和 NPR1 基因或在没有 SA 积累的情况下沉默 NtTTG2 补偿了 NPR1 单基因沉默或缺乏 SA 导致的防御受损。然而,NtTTG2 与 NPR1 不相互作用,但能够调节 NPR1 蛋白的亚细胞定位。在没有 NtTTG2 产生的情况下,NPR1 主要存在于细胞核中,PR 基因表达。相比之下,当 NtTTG2 在转基因植物中积累时,NPR1 的很大一部分被保留在细胞质中,PR 基因不表达。这些结果表明,NtTTG2 通过将 NPR1 从细胞核中隔离出来并抑制防御反应基因的转录激活来抑制 SA/NPR1 调节的防御。

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