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不同的病毒效应子劫持 TCP17,一种宿主生长素合成的关键转录因子,以促进病毒感染。

Different viral effectors hijack TCP17, a key transcription factor for host Auxin synthesis, to promote viral infection.

机构信息

School of Plant Protection, Anhui Agricultural University, Hefei, China.

The Key Laboratory of Plant Immunity, Department of Plant Pathology, Nanjing Agricultural University, Nanjing, China.

出版信息

PLoS Pathog. 2024 Aug 29;20(8):e1012510. doi: 10.1371/journal.ppat.1012510. eCollection 2024 Aug.

Abstract

Auxin is an important class of plant hormones that play an important role in plant growth development, biotic stress response, and viruses often suppress host plant auxin levels to promote infection. However, previous research on auxin-mediated disease resistance has focused mainly on signaling pathway, and the molecular mechanisms of how pathogenic proteins manipulate the biosynthetic pathway of auxin remain poorly understood. TCP is a class of plant-specific transcription factors, of which TCP17 is a member that binds to the promoter of YUCCAs, a key rate-limiting enzyme for auxin synthesis, and promotes the expression of YUCCAs, which is involved in auxin synthesis in plants. In this study, we reported that Tomato spotted wilt virus (TSWV) infection suppressed the expression of YUCCAs through its interaction with TCP17. Further studies revealed that the NSs protein encoded by TSWV disrupts the dimerization of TCP17, thereby inhibit its transcriptional activation ability and reducing the auxin content in plants. Consequently, this interference inhibits the auxin response signal and promotes the TSWV infection. Transgenic plants overexpressing TCP17 exhibit resistance against TSWV infection, whereas plants knocking out TCP17 were more susceptible to TSWV infection. Additionally, proteins encoded by other RNA viruses (BSMV, RSV and TBSV) can also interact with TCP17 and interfere with its dimerization. Notably, overexpression of TCP17 enhanced resistance against BSMV. This suggests that TCP17 plays a crucial role in plant defense against different types of plant viruses that use viral proteins to target this key component of auxin synthesis and promote infection.

摘要

植物激素中的生长素在植物生长发育、生物胁迫响应中起着重要作用,病毒通常会抑制宿主植物生长素水平以促进感染。然而,以前关于生长素介导的抗病性的研究主要集中在信号通路方面,而关于致病蛋白如何操纵生长素生物合成途径的分子机制仍知之甚少。TCP 是一类植物特异性转录因子,其中 TCP17 是一种与 YUCCA 启动子结合的蛋白,YUCCA 是生长素合成的关键限速酶,促进 YUCCA 的表达,从而参与植物中的生长素合成。在这项研究中,我们报告称,番茄斑萎病毒(TSWV)通过与 TCP17 相互作用抑制 YUCCA 的表达。进一步的研究表明,TSWV 编码的 NSs 蛋白破坏 TCP17 的二聚化,从而抑制其转录激活能力并降低植物中的生长素含量。因此,这种干扰抑制了生长素反应信号,促进了 TSWV 的感染。过表达 TCP17 的转基因植物对 TSWV 感染表现出抗性,而敲除 TCP17 的植物对 TSWV 感染更敏感。此外,其他 RNA 病毒(BSMV、RSV 和 TBSV)编码的蛋白也可以与 TCP17 相互作用并干扰其二聚化。值得注意的是,过表达 TCP17 增强了对 BSMV 的抗性。这表明 TCP17 在植物防御不同类型的植物病毒中起着关键作用,这些病毒利用病毒蛋白靶向生长素合成的这个关键组成部分并促进感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9ce/11389919/bd15040bfda1/ppat.1012510.g001.jpg

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