Mol Plant Microbe Interact. 2013 Oct;26(10):1176-89. doi: 10.1094/MPMI-01-13-0019-R.
Pathogenicity of the gram-negative plant-pathogenic bacterium Xanthomonas campestris pv. vesicatoria depends on a membrane-spanning type III secretion (T3S) system, which translocates effector proteins into eukaryotic host cells. In this study, we characterized the T3S system component HrcV, which is a member of the YscV/FlhA family of inner membrane proteins. HrcV consists of eight transmembrane helices and a cytoplasmic region (HrcVC). Mutant and protein-protein interaction studies showed that HrcVC is essential for protein function and binds to T3S substrates, including the early substrate HrpB2, the pilus protein HrpE, and effector proteins. Furthermore, HrcVC interacts with itself and with components and control proteins of the T3S apparatus. The interaction of HrcVC with HrpB2, HrpE, and T3S system components depends on amino acid residues in a conserved motif, designated flagella/hypersensitive response/invasion proteins export pore (FHIPEP), which is located in a cytoplasmic loop between transmembrane helix four and five of HrcV. Mutations in the FHIPEP motif abolish HrcV function but do not affect the interaction of HrcVC with effector proteins.
革兰氏阴性植物病原细菌黄单胞菌 pv.vesicatoria 的致病性取决于一种跨膜 III 型分泌（T3S）系统，该系统将效应蛋白易位到真核宿主细胞中。在这项研究中，我们对 T3S 系统成分 HrcV 进行了表征，HrcV 是内膜蛋白 YscV/FlhA 家族的成员。HrcV 由八个跨膜螺旋和细胞质区域（HrcVC）组成。突变和蛋白-蛋白相互作用研究表明，HrcVC 对于蛋白功能是必需的，并与 T3S 底物结合，包括早期底物 HrpB2、菌毛蛋白 HrpE 和效应蛋白。此外，HrcVC 与自身以及 T3S 装置的组成部分和控制蛋白相互作用。HrcVC 与 HrpB2、HrpE 和 T3S 系统成分的相互作用取决于一个保守基序中的氨基酸残基，该基序被命名为鞭毛/过敏反应/入侵蛋白出口孔（FHIPEP），位于 HrcV 的跨膜螺旋四和五之间的细胞质环中。FHIPEP 基序中的突变会破坏 HrcV 的功能，但不会影响 HrcVC 与效应蛋白的相互作用。
