The fungal pathogen Ustilago maydis targets the maize corepressor RELK2 to modulate host transcription for tumorigenesis. The fungal pathogen Ustilago maydis targets the maize corepressor RELK2 to modulate host transcription for tumorigenesis

Ustilago maydis is a biotrophic fungus that causes tumor formation on all aerial parts of maize. U. maydis secretes effector proteins during penetration and colonization to successfully overcome the plant immune response and reprogram host physiology to promote infection. In this study, we functionally characterized the U. maydis effector protein Topless (TPL) interacting protein 6 (Tip6). We found that Tip6 interacts with the N-terminus of RELK2 through its two Ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motifs. We show that the EAR motifs are essential for the virulence function of Tip6 and critical for altering the nuclear distribution pattern of RELK2. We propose that Tip6 mimics the recruitment of RELK2 by plant repressor proteins, thus disrupting host transcriptional regulation. We show that a large group of AP2/ERF B1 subfamily transcription factors are misregulated in the presence of Tip6. Our study suggests a regulatory mechanism where the U. maydis effector Tip6 utilizes repressive domains to recruit the corepressor RELK2 to disrupt the transcriptional networks of the host plant. Overall design: 9 Samples

玉米黑粉菌（Ustilago maydis）是一种活体营养型真菌，可在玉米的所有地上组织中诱发瘤状病变。该菌在侵入与定殖过程中会分泌效应蛋白，以成功规避植物免疫应答，并重编程宿主生理状态以促进侵染。本研究对玉米黑粉菌效应蛋白Topless（TPL）互作蛋白6（Tip6）进行了功能鉴定。研究发现，Tip6通过其两个乙烯响应元件结合因子相关两亲抑制（EAR）基序，与RELK2的N端结构域发生相互作用。实验表明，EAR基序是Tip6发挥毒力功能的必要条件，同时对改变RELK2的细胞核分布模式至关重要。本研究推测，Tip6可模拟植物阻遏蛋白对RELK2的招募过程，进而干扰宿主的转录调控。实验证实，在Tip6存在时，大量AP2/ERF B1亚家族转录因子出现表达异常调控。本研究提出了一套调控机制：玉米黑粉菌效应蛋白Tip6通过阻遏结构域招募共阻遏蛋白RELK2，从而破坏宿主植物的转录调控网络。实验整体设计：共9个样本。