摘要
Plant stomata close rapidly in response to a rise in the plant hormone abscisic acid(ABA) or salicylic acid(SA) and after recognition of pathogenassociated molecular patterns(PAMPs). Stomatal closure is the result of vacuolar convolution, ion efflux, and changes in turgor pressure in guard cells. Phytopathogenic bacteria secrete type Ⅲ effectors(T3Es) that interfere with plant defense mechanisms, causing severe plant disease symptoms. Here, we show that the virulence and infection of Xanthomonas oryzae pv. oryzicola(Xoc), which is the causal agent of rice bacterial leaf streak disease,drastically increased in transgenic rice(Oryza sativa L.) plants overexpressing the Xoc T3E gene Xop AP, which encodes a protein annotated as a lipase. We discovered that Xop AP binds to phosphatidylinositol 3,5-bisphosphate(Ptd Ins(3,5)P2), a memb rane phospholipid that functions in p H control in lysosomes, membrane dynamics, and protein trafficking. Xop AP inhibited the acidification of vacuoles by competing with vacuolar H+-pyrophosphatase(V-PPase) for binding to Ptd Ins(3,5)P2, leading to stomatal opening. Transgenic rice overexpressing Xop AP also showed inhibition of stomatal closure when challenged by Xoc infection and treatment with the PAMP flg22. Moreover, Xop AP suppressed flg22-induced gene expression, reactive oxygen species burst and callose deposition in host plants, demonstrating that Xop AP subverts PAMP-triggered immunity during Xoc infection. Taken together, these findings demonstrate that Xop AP overcomes stomatal immunity in plants by binding to lipids.
-
单位微生物代谢国家重点实验室; 上海交通大学