Hypermorphic SERK1 Mutations Function via a SOBIR1 Pathway to Activate Floral Abscission Signaling

Abstract

Gain of function mutations in SERK1 suppress the abscission defect of the haesa/haesa-like 2-mutant by activating a SOBIR1 signaling pathway

Abstract

In Arabidopsis ( Arabidopsis thaliana), the abscission of floral organs is regulated by two related receptor-like protein kinases, HAESA (HAE) and HAESA-LIKE2 (HSL2). In complex with members of the SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE (SERK) family of coreceptor protein kinases, HAE and HSL2 are activated when bound by INFLORESCENCE DEFICIENT IN ABSICSSION, a proteolytically processed peptide ligand, activating the expression of genes encoding secreted cell wall remodeling and hydrolase enzymes. hae hsl2 mutants fail to induce expression of these genes and retain floral organs indefinitely. Here, we report identification of an allelic series of hae hsl2 suppressor mutations in the SERK1 coreceptor protein kinase gene. Genetic and transcriptomic evidence indicates that these alleles represent a novel class of gain-of-function mutations that activate signaling independently of HAE/HSL2. We show that, surprisingly, the suppression effect does not rely on the protein kinase activity of SERK1 and that activation of signaling relies on the receptor-like kinase gene SUPPRESSOR OF BIR1 ( SOBIR1). The effect of these mutations can be mimicked by loss of function of BAK1-INTERACTING RECEPTOR-LIKE KINASE1 ( BIR1), a known negative regulator of SERK- SOBIR1 signaling. These results suggest that BIR1 negatively regulates SERK-SOBIR1 signaling during abscission and that the identified SERK1 mutations likely interfere with this negative regulation.