An RxLR effector from Phytophthora infestans prevents re-localisation of two plant NAC transcription factors from the endoplasmic reticulum to the nucleus.
An RxLR effector from Phytophthora infestans prevents re-localisation of two plant NAC transcription factors from the endoplasmic reticulum to the nucleus.
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来自植物疫霉菌的RXLR效应子可防止两个植物NAC转录因子从内质网状到细胞核的重新定位。
DOI：
10.1371/journal.ppat.1003670
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发表时间：
2013
期刊：
影响因子：
6.7
通讯作者：
Birch PR
中科院分区：
文献类型：
--
作者：
McLellan H;Boevink PC;Armstrong MR;Pritchard L;Gomez S;Morales J;Whisson SC;Beynon JL;Birch PR
马铃薯晚疫病病原体致病疫霉（Phytophthora infestans）分泌一系列效应蛋白，被认为通过解除防御和促进病原体定殖来在其宿主中起作用。然而，对这些效应物的宿主靶点以及它们如何被病原体操纵知之甚少。这项工作描述了两个推定的膜相关的NAC转录因子（TF）作为RxLR效应PITG_03192（Pi 03192）的宿主靶标的鉴定。效应子与定位于内质网（ER）膜上的疫霉靶向NAC（NTP）1和NTP 2相互作用。NTP 1和NTP 2的转录物在用来自体外生长的致病疫霉的培养物滤液（CF）处理后迅速积累，其充当疫霉PAMP和激发子的混合物，但在致病疫霉感染期间显著降低，表明病原体活性可能阻止它们的上调。模式宿主植物本氏烟草中NTP 1或NTP 2的沉默增加了对致病疫霉的易感性，而致病疫霉中Pi 03192的沉默降低了致病性。Pi 03192在植物中的瞬时表达恢复了Pi 03192沉默系的致病性。此外，Pi 03192沉默株系在N.在本氏植物中，NTP 1或NTP 2已经沉默。StNTP 1和StNTP 2蛋白在用致病疫霉CF处理后从ER膜释放并在细胞核中积累，之后它们被26 S蛋白酶体快速翻转。相比之下，用限定的PAMP flg 22处理不能上调NTP 1和NTP 2，或促进其蛋白产物重新定位到细胞核，表明这些事件遵循似乎独立于FLS 2/flg 22途径的CF组分的感知。重要的是，Pi 03192阻止了CF触发的StNTP 1和StNTP 2从ER重新定位到细胞核中，揭示了一种促进疾病进展的新型效应器作用模式。植物免疫系统在感知到被识别为非自我的暴露的、必需的和不变的微生物分子后被激活。植物免疫的一个主要组成部分是参与广泛防御反应的基因的转录诱导。反过来，适应的病原体传递效应蛋白，这些效应蛋白在植物细胞内或外发挥作用，通常通过它们对植物蛋白靶标的直接作用来操纵宿主过程。迄今为止，很少有效应子被证明直接操纵植物防御的转录调节因子。此外，很少有人知道一般的丝状（真菌和卵菌）植物病原体的效应的作用方式。我们描述了一个效应器，称为Pi 03192，从晚疫病病原体致病疫霉，它与一对宿主转录因子在内质网（ER）内的植物细胞相互作用。我们表明，这些转录因子从ER释放进入细胞核，病原体的感知，并在限制疾病是重要的。Pi 03192阻止植物转录因子在寄主细胞核中的积累，揭示了一种增强寄主易感性的新方法。
The potato late blight pathogen Phytophthora infestans secretes an array of effector proteins thought to act in its hosts by disarming defences and promoting pathogen colonisation. However, little is known about the host targets of these effectors and how they are manipulated by the pathogen. This work describes the identification of two putative membrane-associated NAC transcription factors (TF) as the host targets of the RxLR effector PITG_03192 (Pi03192). The effector interacts with NAC Targeted by Phytophthora (NTP) 1 and NTP2 at the endoplasmic reticulum (ER) membrane, where these proteins are localised. Transcripts of NTP1 and NTP2 rapidly accumulate following treatment with culture filtrate (CF) from in vitro grown P. infestans, which acts as a mixture of Phytophthora PAMPs and elicitors, but significantly decrease during P. infestans infection, indicating that pathogen activity may prevent their up-regulation. Silencing of NTP1 or NTP2 in the model host plant Nicotiana benthamiana increases susceptibility to P. infestans, whereas silencing of Pi03192 in P. infestans reduces pathogenicity. Transient expression of Pi03192 in planta restores pathogenicity of the Pi03192-silenced line. Moreover, colonisation by the Pi03192-silenced line is significantly enhanced on N. benthamiana plants in which either NTP1 or NTP2 have been silenced. StNTP1 and StNTP2 proteins are released from the ER membrane following treatment with P. infestans CF and accumulate in the nucleus, after which they are rapidly turned over by the 26S proteasome. In contrast, treatment with the defined PAMP flg22 fails to up-regulate NTP1 and NTP2, or promote re-localisation of their protein products to the nucleus, indicating that these events follow perception of a component of CF that appears to be independent of the FLS2/flg22 pathway. Importantly, Pi03192 prevents CF-triggered re-localisation of StNTP1 and StNTP2 from the ER into the nucleus, revealing a novel effector mode-of-action to promote disease progression. The plant immune system is activated following the perception of exposed, essential and invariant microbial molecules that are recognised as non-self. A major component of plant immunity is the transcriptional induction of genes involved in a wide array of defence responses. In turn, adapted pathogens deliver effector proteins that act either inside or outside plant cells to manipulate host processes, often through their direct action on plant protein targets. To date, few effectors have been shown to directly manipulate transcriptional regulators of plant defence. Moreover, little is known generally about the modes of action of effectors from filamentous (fungal and oomycete) plant pathogens. We describe an effector, called Pi03192, from the late blight pathogen Phytophthora infestans, which interacts with a pair of host transcription factors at the endoplasmic reticulum (ER) inside plant cells. We show that these transcription factors are released from the ER to enter the nucleus, following pathogen perception, and are important in restricting disease. Pi03192 prevents the plant transcription factors from accumulating in the host nucleus, revealing a novel means of enhancing host susceptibility.
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影响因子：
11.6
作者：
Ishihama, Nobuaki;Yamada, Reiko;Yoshioka, Hirofumi
通讯作者：
Yoshioka, Hirofumi
影响因子：
11.6
作者：
Dou, Daolong;Kale, Shiv D.;Tyler, Brett M.
通讯作者：
Tyler, Brett M.
DOI：
10.1093/bioinformatics/btp348
发表时间：
2009-08-01
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Capella-Gutiérrez S;Silla-Martínez JM;Gabaldón T
通讯作者：
Gabaldón T
影响因子：
5.4
作者：
Block A;Alfano JR
通讯作者：
Alfano JR
DOI：
10.1073/pnas.1112708109
发表时间：
2011-12-20
影响因子：
11.1
作者：
Bozkurt, Tolga O.;Schornack, Sebastian;Kamoun, Sophien
通讯作者：
Kamoun, Sophien