The SERK1 receptor-like kinase regulates organ separation in Arabidopsis flowers

Abstract

SUMMARYThrough a sensitized screen for novel components of pathways regulating organ separation in Arabidopsis flowers, we have found that the leucine-rich repeat receptor-like kinase SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE1 (SERK1) acts as a negative regulator of abscission. Mutations in SERK1 dominantly rescue abscission in flowers without functional NEVERSHED (NEV), an ADP-ribosylation factor GTPaseactivating protein required for floral organ shedding. We previously reported that the organization of the Golgi apparatus and location of the trans-Golgi network (TGN) are altered in nev mutant flowers. Disruption of SERK1 restores Golgi structure and the close association of the TGN in nev flowers, suggesting that defects in these organelles may be responsible for the block in abscission. We have also found that the abscission zones of nev serk1 flowers are enlarged compared to wild-type. A similar phenotype was previously observed in plants constitutively expressing a putative ligand required for organ separation, INFLORESCENCE DEFICIENT IN ABSCISSION (IDA), suggesting that signalling through IDA and its proposed receptors, HAESA and HAESA-LIKE2, may be deregulated in nev serk1 abscission zone cells. Our studies indicate that in addition to its previously characterized roles in stamen development and brassinosteroid perception, SERK1 plays a unique role in modulating the loss of cell adhesion that occurs during organ abscission.

CAST AWAY, a Membrane-Associated Receptor-Like Kinase, Inhibits Organ Abscission in Arabidopsis

“…2F). Enlarged AZs that form visible collars of rough tissue are also found in nev evr, nev serk1, and 35S::IDA flowers instead of the smooth, discrete AZ scars of the wild type (Stenvik et al, 2006;Leslie et al, 2010;Lewis et al, 2010). The remarkable similarity of these phenotypes suggests that the rescue of organ abscission, AZ enlargement, and AZ boundary blurring in nev cst flowers may be due to ectopic, prolonged signaling of HAE and HSL2, the putative receptors of the IDA peptide.…”

“…As an ARF-GAP, NEV may regulate the activity and recruitment of the same TGN-localized ARF G-protein(s) and adaptor molecules as the V-ATPase complex. The significant rescue of extracellular vesicle defects in nev cst flowers, which was not observed in nev serk1 or nev evr flowers Lewis et al, 2010), suggests the possibility that CST may interact more directly with NEV and in a different manner from EVR and SERK1 to inhibit abscission. Alternatively, if EVR and SERK1 act redundantly, suppression of extracellular vesicle accumulation may also be observed in nev serk1 evr flowers.…”

“…Recent studies have shown that the concanamycin A-induced structures are labeled with VHA-a1 and SYP61, markers of the TGN/early endosome (Viotti et al, 2010). These results suggest the possibility that the circularized structures in nev flowers are also chimeric fusions of the Golgi cisternae and the TGN and that traffic through the TGN/early endosome is affected by mutations in NEV. Disruption of CST, EVR, or SERK1 activity appears to restore the identity and independence of the TGN from the Golgi in nev flowers Lewis et al, 2010). Defects in membrane trafficking are thought to underlie the inappropriate fusion of the TGN and the Golgi, as V-ATPase-mediated endomembrane acidification is required to recruit ARF G-proteins, ARF-GEFs, and coat components involved in vesicle budding (Zeuzem et al, 1992;Aniento et al, 1996;Maranda et al, 2001;Hurtado-Lorenzo et al, 2006;Viotti et al, 2010).…”

“…Like the EVR and SERK1 LRRRLKs Lewis et al, 2010), CST appears to restrict the extent of cell separation signaling, such that only cells within designated domains at the base of each outer organ undergo cell loosening, separation, and expansion. In nev cst flowers, the boundaries between the individual organ attachment sites and the border with the floral pedicel become notably obscured after organ abscission (Fig.…”

“…The predicted signaling ligand for HAE/ HSL2 is INFLORESCENCE DEFICIENT IN ABSCIS-SION (IDA), a small, secreted peptide (Butenko et al, 2003;Cho et al, 2008;Stenvik et al, 2008). Two inhibitors of organ separation that may directly regulate HAE/HSL2 are the EVERSHED (EVR) and SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE1 (SERK1) LRR-RLKs Lewis et al, 2010). Mutations in EVR or SERK1 were found to restore abscission in plants defective for NEVERSHED (NEV), a gene that encodes an ADP-ribosylation factor GTPase-activating protein (ARF-GAP).…”