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疫霉属 RXLR 效应因子 SFI5 需要与钙调蛋白结合才能发挥抑制 PTI/MTI 的活性。

Phytophthora infestans RXLR effector SFI5 requires association with calmodulin for PTI/MTI suppressing activity.

机构信息

Department of Biochemistry, Centre for Plant Molecular Biology, Eberhard Karls University, Auf der Morgenstelle 32, D-72076, Tübingen, Germany.

Center for Molecular Cell and Systems Biology, College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

出版信息

New Phytol. 2018 Sep;219(4):1433-1446. doi: 10.1111/nph.15250. Epub 2018 Jun 22.

Abstract

Pathogens secrete effector proteins to interfere with plant innate immunity, in which Ca /calmodulin (CaM) signalling plays key roles. Thus far, few effectors have been identified that directly interact with CaM for defence suppression. Here, we report that SFI5, an RXLR effector from Phytophthora infestans, suppresses microbe-associated molecular pattern (MAMP)-triggered immunity (MTI) by interacting with host CaMs. We predicted the CaM-binding site in SFI5 using in silico analysis. The interaction between SFI5 and CaM was tested by both in vitro and in vivo assays. MTI suppression by SFI5 and truncated variants were performed in a tomato protoplast system. We found that both the predicted CaM-binding site and the full-length SFI5 protein interact with CaM in the presence of Ca . MTI responses, such as FRK1 upregulation, reactive oxygen species accumulation, and mitogen-activated protein kinase activation were suppressed by truncated SFI5 proteins containing the C-terminal CaM-binding site but not by those without it. The plasma membrane localization of SFI5 and its ability to enhance infection were also perturbed by loss of the CaM-binding site. We conclude that CaM-binding is required for localization and activity of SFI5. We propose that SFI5 suppresses plant immunity by interfering with immune signalling components after activation by CaMs.

摘要

病原体分泌效应蛋白来干扰植物先天免疫,其中 Ca/钙调蛋白 (CaM) 信号转导起着关键作用。迄今为止,很少有被鉴定的效应子可以直接与 CaM 相互作用以抑制防御。在这里,我们报告了来自马铃薯晚疫病菌的 RXLR 效应子 SFI5 通过与宿主 CaMs 相互作用来抑制微生物相关分子模式 (MAMP) 触发的免疫 (MTI)。我们使用计算机分析预测了 SFI5 中的 CaM 结合位点。通过体外和体内测定测试了 SFI5 和 CaM 之间的相互作用。在番茄原生质体系统中进行了 SFI5 和截短变体对 MTI 的抑制作用。我们发现,在 Ca 存在的情况下,预测的 CaM 结合位点和全长 SFI5 蛋白都与 CaM 相互作用。包含 C 末端 CaM 结合位点的截短 SFI5 蛋白可以抑制 FRK1 的上调、活性氧物质的积累和丝裂原活化蛋白激酶的激活等 MTI 反应,但没有该位点的截短 SFI5 蛋白则不能。SFI5 的质膜定位及其增强感染的能力也因 CaM 结合位点的缺失而受到干扰。我们得出结论,CaM 结合对于 SFI5 的定位和活性是必需的。我们提出,SFI5 通过与 CaM 激活后干扰免疫信号成分来抑制植物免疫。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/306c/6099356/d9a982979199/NPH-219-1433-g001.jpg

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