AUTHOR=Wu Wangze , Wu Yujun , Gao Yang , Li Meizhen , Yin Hongju , Lv Minghui , Zhao Jianxin , Li Jia , He Kai 

TITLE=Somatic embryogenesis receptor-like kinase 5 in the ecotype Landsberg erecta of Arabidopsis is a functional RD LRR-RLK in regulating brassinosteroid signaling and cell death control

JOURNAL=Frontiers in Plant Science

VOLUME=6

YEAR=2015

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2015.00852

DOI=10.3389/fpls.2015.00852

ISSN=1664-462X

ABSTRACT=<p>In plants, LRR-RLKs play central roles in regulating perception of extracellular signals and initiation of cellular responses under various environmental challenges. <italic>Arabidopsis SERK</italic> genes, including <italic>SERK1</italic> to <italic>SERK5</italic>, constitute a <italic>LRR</italic>-<italic>RLK</italic> sub-family. <italic>SERK1, SERK2, SERK3</italic>/<italic>BAK1</italic>, and <italic>SERK4</italic>/<italic>BKK1</italic> have been well characterized to function as crucial regulators in multiple physiological processes such as brassinosteroid signaling, cell death control, pathogenesis, and pollen development. Despite extremely high sequence identity with <italic>BKK1, SERK5</italic> is reported to have no functional overlapping with <italic>BKK1</italic>, which is previously identified to regulate BR and cell death control pathways, probably due to a natural mutation in a highly conserved RD motif in the kinase domain of SERK5 in Col-0 ecotype. Through a gene sequencing analysis in several <italic>Arabidopsis</italic> accessions, we are able to identify <italic>SERK5</italic> in Landsberg <italic>erecta</italic> (L<italic>er</italic>) genome encoding a LRR-RLK with an intact RD motif. Overexpression of <italic>SERK5</italic>-L<italic>er</italic> partially suppresses the BR defective phenotypes of <italic>bri1-5</italic> and <italic>bak1-3 bkk1-1</italic>, indicating <italic>SERK5</italic>-L<italic>er</italic> functions as a positive regulator in BR signaling. Furthermore, the interaction between SERK5-L<italic>er</italic> and BRI1 is confirmed by yeast two-hybrid and BiFC assays, and the genetic result showing that elevated expression of a kinase-dead form of <italic>SERK5</italic>-L<italic>er</italic> causes a dominant-negative phenotype in <italic>bri1-5</italic>. In addition, overexpression of <italic>SERK5</italic>-L<italic>er</italic> is capable of delaying, not completely suppressing, the cell death phenotype of <italic>bak1-3 bkk1-1</italic>. In this study, we first reveal that <italic>SERK5</italic>-L<italic>er</italic> is a biologically functional component in mediating multiple signaling pathways.</p>