Li Peng, Xie Lizhu, Li Wen, Zhou Gangqiang, Situ Junjian, Zhang Zijing, Li Minhui, Xi Pinggen, Jiang Zide, Kong Guanghui
National Key Laboratory of Green Pesticide/Guangdong Province Key Laboratory of Microbial Signals and Disease Control, South China Agricultural University, Guangzhou, 510642, China.
State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, College of Agriculture, Guangxi University, Nanning, 530004, China.
Plant J. 2025 Sep;123(5):e70457. doi: 10.1111/tpj.70457.
Tropical and subtropical fruit trees face serious threats of oomycete-caused plant diseases. However, the molecular mechanism by which oomycete pathogens suppress the immunity of these fruit trees remains largely unclear. Effectors play a crucial role in the pathogenesis of plant pathogenic oomycetes. Here, we found that a conserved RXLR-type effector protein PlAvh222 from the pathogen Peronophythora litchii is required for its full virulence on litchi. Expression of PlAvh222 in Nicotiana benthamiana leaves suppressed INF1-induced immune responses and promoted Phytophthora capsici infection. Further research demonstrated that PlAvh222 interacted with litchi calmodulins (LcCaMs) in vivo and in vitro. Silencing of NbCaM1/2/3/4 attenuated the ability of PlAvh222 to enhance N. benthamiana susceptibility. The C-terminal CaM-binding region of PlAvh222 is required for targeting LcCaM and to suppress N. benthamiana immune responses, including programmed cell death (PCD) and reactive oxygen species (ROS) burst. In addition, the interaction between PlAvh222 and LcCaM1/2/3 increases the accumulation of LcCaM1/2/3 and reduces levels of cytosolic Ca ([Ca]). Blocking [Ca] influx leads to compromised PCD in N. benthamiana. Our results reveal that the oomycete effector promotes pathogen infection through suppressing [Ca]-induced plant immunity.
热带和亚热带果树面临着卵菌引起的植物病害的严重威胁。然而，卵菌病原体抑制这些果树免疫的分子机制仍不清楚。效应子在植物病原卵菌的致病过程中起着关键作用。在此，我们发现病原菌荔枝霜霉病菌中一个保守的RXLR型效应子蛋白PlAvh222对其在荔枝上的完全致病性是必需的。PlAvh222在本氏烟草叶片中的表达抑制了INF1诱导的免疫反应，并促进了辣椒疫霉的感染。进一步研究表明，PlAvh222在体内和体外与荔枝钙调蛋白（LcCaMs）相互作用。沉默NbCaM1/2/3/4减弱了PlAvh222增强本氏烟草易感性的能力。PlAvh222的C末端钙调蛋白结合区域是靶向LcCaM并抑制本氏烟草免疫反应所必需的，包括程序性细胞死亡（PCD）和活性氧（ROS）爆发。此外，PlAvh222与LcCaM1/2/3之间的相互作用增加了LcCaM1/2/3的积累，并降低了胞质钙（[Ca]）水平。阻断[Ca]内流导致本氏烟草中PCD受损。我们的结果表明，卵菌效应子通过抑制[Ca]诱导的植物免疫来促进病原菌感染。
