Shanzhi Wang, Lisong Zhu, Meng Tian, Wenyi Wu, Xu Hu, Xuan Li, Jiyang Wang, Ying Zhu, Jiaqing Xu, Baohui Mou, Jiyun Yang, Fuhao Cui, Dayong Li, Jie Cheng, Zhi Long Liu, Mingan Wang, Linlu Qi, Weiwei Jin, Zhao‐Qing Luo, Pei Zhou, Yong‐Hwan Lee, Brian J. Staskawicz, Sheng Yang He, Wenxian Sun
Xanthomonas spp. cause serious diseases in more than 400 plant species. The conserved AvrBs2 family effectors are among the most important virulence factors in xanthomonads, but how AvrBs2 promotes infection remains elusive. We found that AvrBs2 is a glycerophosphodiesterase-derived synthetase that catalyzes uridine 5′-diphosphate-α- d -galactose into a sugar phosphodiester, bis-(1,6)-cyclic dimeric α- d -galactose-phosphate, which is referred to as xanthosan. Xanthosan is synthesized by AvrBs2 in host cells and released into apoplastic spaces. Xanthomonas bacteria uptake xanthosan through the XanT transporter and hydrolyze it through the XanP phosphodiesterase for nutrition. AvrBs2, XanT, and XanP form a xanthosan “generation-uptake-utilization” system to provide a dedicated nutritional strategy to feed xanthomonads. Furthermore, elucidation of the AvrBs2-XanT-XanP virulence mechanism inspired us to develop an “anti-nutrition” strategy that should be applicable to control a wide variety of Xanthomonas diseases.