Hatsugai Noriyuki, Hillmer Rachel, Yamaoka Shohei, Hara-Nishimura Ikuko, Katagiri Fumiaki
1 Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, 1500 Gortner Ave., St. Paul, MN 55108, U.S.A.; and.
2 Department of Botany, Graduate School of Science, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto 606-8502, Japan.
Mol Plant Microbe Interact. 2016 May;29(5):345-51. doi: 10.1094/MPMI-10-15-0228-R. Epub 2016 Mar 29.
Endocytosis has been suggested to be important in the cellular processes of plant immune responses. However, our understanding of its role during effector-triggered immunity (ETI) is still limited. We have previously shown that plant endocytosis, especially clathrin-coated vesicle formation at the plasma membrane, is mediated by the adaptor protein-2 (AP-2) complex and that loss of the μ subunit of AP-2 (AP2M) affects plant growth and floral organ development. Here, we report that AP2M is required for full-strength ETI mediated by the disease resistance (R) genes RPM1 and RPS2 in Arabidopsis. Reduced ETI was observed in an ap2m mutant plant, measured by growth of Pseudomonas syringae pv. tomato DC3000 strains carrying the corresponding effector genes avrRpm1 or avrRpt2 and by hypersensitive cell death response and defense gene expression triggered by these strains. In contrast, RPS4-mediated ETI and its associated immune responses were not affected by the ap2m mutation. While RPM1 and RPS2 are localized to the plasma membrane, RPS4 is localized to the cytoplasm and nucleus. Our results suggest that AP2M is involved in ETI mediated by plasma membrane-localized R proteins, possibly by mediating endocytosis of the immune receptor complex components from the plasma membrane.
内吞作用被认为在植物免疫反应的细胞过程中很重要。然而，我们对其在效应物触发免疫（ETI）过程中的作用的理解仍然有限。我们之前已经表明，植物内吞作用，尤其是质膜上网格蛋白包被囊泡的形成，是由衔接蛋白-2（AP-2）复合物介导的，并且AP-2的μ亚基（AP2M）缺失会影响植物生长和花器官发育。在这里，我们报道AP2M是拟南芥中由抗病（R）基因RPM1和RPS2介导的完全强度ETI所必需的。在ap2m突变体植物中观察到ETI减弱，通过携带相应效应物基因avrRpm1或avrRpt2的丁香假单胞菌番茄致病变种DC3000菌株的生长以及这些菌株触发的过敏细胞死亡反应和防御基因表达来衡量。相比之下，RPS4介导的ETI及其相关免疫反应不受ap2m突变的影响。虽然RPM1和RPS2定位于质膜，但RPS4定位于细胞质和细胞核。我们的结果表明，AP2M参与由质膜定位的R蛋白介导的ETI，可能是通过介导免疫受体复合物组分从质膜的内吞作用。
