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 triple null mutant exhibits an extreme de-etiolated phenotype similar to a null bri1 mutant. While overexpression of BRI1 can drastically increase hypocotyl growth of wild-type plants, overexpression of BRI1 does not alter hypocotyl growth of the serk1 bak1 bkk1 triple mutant. Biochemical analysis indicated that the phosphorylation level of BRI1 in serk1 bak1 bkk1 is incapable of sensing exogenously applied BR. As a result, the unphosphorylated level of BES1 has lost its sensitivity to the BR treatment in the triple mutant, indicating that the BR signaling pathway has been completely abolished in the triple mutant. These data clearly demonstrate that SERKs are essential to the early events of BR signaling.
Highlights
Brassinosteroids (BRs) are naturally produced plant hormones regulating many developmental processes from seed germination to flowering and senescence [1]
SERK1, SERK2, Brassinosteroid Insensitive 1 (BRI1)-Associated Receptor Kinase 1 (BAK1), and BAK1-Like 1 (BKK1) are the only members in the leucine-rich repeat receptor-like protein kinase (LRR-RLK) II subfamily which can suppress bri1-5 when overexpressed
Our results indicated that only SERK1, SERK2, BAK1, and BKK1 could partially suppress bri1-5 phenotypes when overexpressed (Figure 1B)
Summary
Brassinosteroids (BRs) are naturally produced plant hormones regulating many developmental processes from seed germination to flowering and senescence [1]. BR deficiency or response mutants show typical phenotypic defects including decreased rate of seed germination, rounded and epinastic rosette leaves, extremely dwarfed stature, delayed flowering time, reduced male fertility, postponed leaf senescence, and extremely de-etiolated phenotypes grown under dark conditions [2,3,4,5]. Both plants and animals use steroids as growth regulators, the signaling pathways in the two kingdoms are divergent [6]. The ligand-receptor interaction initiates the BR signaling cascade, mostly via reversible phosphorylation and dephosphorylation [16]
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