Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, Nanjing, China.
Key Laboratory of Integrated Management of Crop Diseases and Pests, Ministry of Education, Nanjing, China.
mBio. 2020 Mar 24;11(2):e03304-19. doi: 10.1128/mBio.03304-19.
The appressoria that are generated by the rice blast fungus in response to surface cues are important for successful colonization. Previous work showed that regulators of G-protein signaling (RGS) and RGS-like proteins play critical roles in appressorium formation. However, the mechanisms by which these proteins orchestrate surface recognition for appressorium induction remain unclear. Here, we performed comparative transcriptomic studies of Δ mutant and wild-type strains and found that Aa91 (MoAa91), a homolog of the auxiliary activity family 9 protein (Aa9), was required for surface recognition of We found that was regulated by the MoMsn2 transcription factor and that its disruption resulted in defects in both appressorium formation on the artificial inductive surface and full virulence of the pathogen. We further showed that MoAa91 was secreted into the apoplast space and was capable of competing with the immune receptor chitin elicitor-binding protein precursor (CEBiP) for chitin binding, thereby suppressing chitin-induced plant immune responses. In summary, we have found that MoAa91 is a novel signaling molecule regulated by RGS and RGS-like proteins and that MoAa91 not only governs appressorium development and virulence but also functions as an effector to suppress host immunity. The rice blast fungus generates infection structure appressoria in response to surface cues largely due to functions of signaling molecules, including G-proteins, regulators of G-protein signaling (RGS), mitogen-activated protein (MAP) kinase pathways, cAMP signaling, and TOR signaling pathways. encodes eight RGS and RGS-like proteins (MoRgs1 to MoRgs8), and MoRgs1, MoRgs3, MoRgs4, and MoRgs7 were found to be particularly important in appressorium development. To explore the mechanisms by which these proteins regulate appressorium development, we have performed a comparative transcriptomic study and identified an uxiliary ctivity family 9 protein (Aa9) homolog that we named MoAa91. We showed that MoAa91 was secreted from appressoria and that the recombinant MoAa91 could compete with a chitin elicitor-binding protein precursor (CEBiP) for chitin binding, thereby suppressing chitin-induced plant immunity. By identifying MoAa91 as a novel signaling molecule functioning in appressorium development and an effector in suppressing host immunity, our studies revealed a novel mechanism by which RGS and RGS-like proteins regulate pathogen-host interactions.
稻瘟病菌产生的附着胞对表面线索的反应对于成功定殖很重要。先前的工作表明，G 蛋白信号转导调节剂（RGS）和 RGS 样蛋白在附着胞形成中发挥关键作用。然而，这些蛋白协调表面识别以诱导附着胞形成的机制尚不清楚。在这里，我们对Δ突变体和野生型菌株进行了比较转录组研究，发现 Aa91（MoAa91），一种辅助活性家族 9 蛋白（Aa9）的同源物，是表面识别所必需的诱导附着胞。我们发现被 MoMsn2 转录因子调控，其缺失导致在人工诱导表面上形成附着胞和病原体完全毒力的缺陷。我们进一步表明，MoAa91分泌到质外体空间，并能够与免疫受体几丁质结合蛋白前体（CEBiP）竞争几丁质结合，从而抑制几丁质诱导的植物免疫反应。总之，我们发现 MoAa91 是一种受 RGS 和 RGS 样蛋白调控的新型信号分子，MoAa91 不仅控制附着胞发育和毒力，而且作为一种效应子抑制宿主免疫。稻瘟病菌 产生感染结构附着胞以响应表面线索，这在很大程度上归因于信号分子的功能，包括 G 蛋白、G 蛋白信号转导调节剂（RGS）、丝裂原活化蛋白（MAP）激酶途径、cAMP 信号转导和 TOR 信号转导途径。 编码八个 RGS 和 RGS 样蛋白（MoRgs1 至 MoRgs8），并且发现 MoRgs1、MoRgs3、MoRgs4 和 MoRgs7 在附着胞发育中特别重要。为了探讨这些蛋白调节附着胞发育的机制，我们进行了比较 转录组研究，鉴定出一个辅助活性家族 9 蛋白（Aa9）同源物，我们将其命名为 MoAa91。我们表明 MoAa91 从附着胞中分泌出来，重组的 MoAa91 可以与几丁质结合蛋白前体（CEBiP）竞争几丁质结合，从而抑制几丁质诱导的植物免疫。通过鉴定 MoAa91 作为一种新型信号分子，在附着胞发育中发挥作用，并作为一种抑制宿主免疫的效应子，我们的研究揭示了 RGS 和 RGS 样蛋白调节病原体-宿主相互作用的新机制。
