type iii effector activation via nucleotide binding, phosphorylation, and host target interaction类型iii效应通过核苷酸绑定激活,磷酸化和主机目标交互.pdfVIP

Type III Effector Activation via Nucleotide Binding, Phosphorylation, and Host Target Interaction 1[¤a 2[¤b 1[ 1[ 1 1 Darrell Desveaux , Alex U. Singer , Ai-Jiuan Wu , Brian C. McNulty , Laura Musselwhite , Zachary Nimchuk , John Sondek2,3,4, Jeffery L. Dangl 1,5,6,7* 1 Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 2 Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 3 Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 4 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 5 Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 6 Curriculum in Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 7 Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America The Pseudomonas syringae type III effector protein avirulence protein B (AvrB) is delivered into plant cells, where it targets the Arabidopsis RIN4 protein (resistance to Pseudomonas maculicula protein 1 [RPM1]–interacting protein). RIN4 is a regulator of basal host defense responses. Targeting of RIN4 by AvrB is recognized by the host RPM1 nucleotide- binding leucine-rich repeat disease resistance protein, leading to accelerated defense resp