genetic evidence for an indispensable role of somatic embryogenesis receptor kinases in brassinosteroid signaling遗传证据不可或缺的角色brassinosteroid体细胞胚胎发生受体激酶的信号.pdfVIP

Genetic Evidence for an Indispensable Role of Somatic Embryogenesis Receptor Kinases in Brassinosteroid Signaling 1. 1. 2. 1,3 1 1 3 Xiaoping Gou , Hongju Yin , Kai He , Junbo Du , Jing Yi , Shengbao Xu , Honghui Lin , Steven D. Clouse4, Jia Li1,2* 1 School of Life Sciences, Lanzhou University, Lanzhou, China, 2 Department of Botany and Microbiology, University of Oklahoma, Norman, Oklahoma, United States of America, 3 School of Life Sciences, Sichuan University, Chengdu, China, 4 Department of Horticultural Science, North Carolina State University, Raleigh, North Carolina, United States of America Abstract The Arabidopsis thaliana Somatic Embryogenesis Receptor Kinases (SERKs) consist of five members, SERK1 to SERK5, of the leucine-rich repeat receptor-like kinase subfamily II (LRR-RLK II). SERK3 was named BRI1-Associated Receptor Kinase 1 (BAK1) due to its direct interaction with the brassinosteroid (BR) receptor BRI1 in vivo, while SERK4 has also been designated as BAK1-Like 1 (BKK1) for its functionally redundant role with BAK1. Here we provide genetic and biochemical evidence to demonstrate that SERKs are absolutely required for early steps in BR signaling. Overexpression of four of the five SERKs— SERK1, SERK2, SERK3/BAK1, and SERK4/BKK1—suppressed the phenotypes of an intermediate BRI1 mutant, bri1-5. Overexpression of the kinase-dead versions of these four genes in the bri1-5 background, on the other hand, resulted in typical dominant negative phenotypes, resembling those of null BRI1 mutants. We isolated and generated single, double, triple, and quadruple mutants and analyzed their phenotypes in detail. While the quadruple mutant is embryo-lethal, the serk1 bak1 bkk1 tr