Phytophthora spp. secrete vast arrays of effector molecules during infection to aid in host colonization. The crinkling and necrosis (CRN) protein family forms an extensive repertoire of candidate effectors that accumulate in the host nucleus to perturb processes required for immunity. Here, we show that CRN12_997 from Phytophthora capsici binds a TCP transcription factor, SlTCP14-2, to inhibit its immunity-associated activity against Phytophthora spp. Coimmunoprecipitation and bimolecular fluorescence complementation studies confirm a specific CRN12_997-SlTCP14-2 interaction in vivo. Coexpression of CRN12_997 specifically counteracts the TCP14-enhanced immunity phenotype, suggesting that CRN mediated perturbation of SlTCP14-2 function. We show that SlTCP14-2 associates with nuclear chromatin and that CRN12_997 diminishes SlTCP14-2 DNA binding. Collectively, our data support a model in which SlTCP14-2 associates with chromatin to enhance immunity. The interaction between CRN12_997 and SlTCP14-2 reduces DNA binding of the immune regulator. We propose that the modulation of SlTCP14-2 chromatin affinity, caused by CRN12-997, enhances susceptibility to P. capsici.

Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

疫霉属 在感染过程中会分泌大量效应分子，以帮助宿主定植。皱纹和坏死（CRN）蛋白家族形成了候选效应子的广泛库，这些效应子积聚在宿主细胞核中，扰乱了免疫所需的过程。在这里，我们显示来自辣椒疫霉菌的CRN12_997结合TCP转录因子SlTCP14-2，以抑制其针对疫霉菌的免疫相关活性spp。免疫共沉淀和双分子荧光互补研究证实了体内特定的CRN12_997-S1TCP14-2相互作用。CRN12_997的共表达特异性抵消了TCP14增强的免疫表型，表明CRN介导了SlTCP14-2功能的扰动。我们显示SlTCP14-2与核染色质相关联，并且CRN12_997减少了SlTCP14-2 DNA的结合。总体而言，我们的数据支持一个模型，其中SlTCP14-2与染色质相关联以增强免疫力。CRN12_997和SlTCP14-2之间的相互作用减少了免疫调节剂的DNA结合。我们建议SlTCP14-2染色质亲和力的调节，造成CRN12-997，提高易感辣椒疫霉。

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