The EVERSHED receptor-like kinase modulates floral organ shedding inArabidopsis

Abstract

Plant cell signaling triggers the abscission of entire organs, such as fruit, leaves and flowers. Previously, we characterized an ADP-ribosylation factor GTPase-activating protein, NEVERSHED (NEV), that regulates membrane trafficking and is essential for floral organ shedding in Arabidopsis. Through a screen for mutations that restore organ separation in nev flowers, we have identified a leucine-rich repeat receptor-like kinase, EVERSHED (EVR), that functions as an inhibitor of abscission. Defects in the Golgi structure and location of the trans-Golgi network in nev abscission zone cells are rescued by a mutation in EVR, suggesting that EVR might regulate membrane trafficking during abscission. In addition to shedding their floral organs prematurely, nev evr flowers show enlarged abscission zones. A similar phenotype was reported for plants ectopically expressing INFLORESCENCE DEFICIENT IN ABSCISSION, a predicted signaling ligand for the HAESA/HAESA-LIKE2 receptor-like kinases, indicating that this signaling pathway may be constitutively active in nev evr flowers. We present a model in which EVR modulates the timing and region of abscission by promoting the internalization of other receptor-like kinases from the plasma membrane.

Four shades of detachment: Regulation of floral organ abscission

“…It was concluded that these suppressors act downstream of NEV to spatially inhibit organ separation. [9][10][11] Notably, mutations in these 3 receptor-like kinases did not restore the phenotype in either the ida or hae hsl2 mutants. [9][10][11] Additionally, whereas the defects of abscission and the Golgi network in the nev mutants are rescued by these suppressors, the ectopic cell expansion of nev in late abscission remained unaffected in the double mutants (nev-3 evr, nev-3 serk1, nev-3 cst) and the triple mutants (nev-3 serk1 ida-2 and nev-3 ever-2 ida-2).…”

“…NEVERSHED (NEV) encodes an ADP-ribosylation factor-GTPase activating protein (ARF-GAP) that appears to regulate the movement of molecules leaving the trans-Golgi network and/or cycling between the cell surface and endosomes. [8][9][10][11] Mutations in NEV result in membrane trafficking defects and inhibition of abscission. 8 Whereas nev mutants display distinct uncontrolled cell expansion late in abscission, the AZ cell morphology early in abscission is similar to ida mutants and appears to be normal.…”

“…[9][10][11] In addition to the abscission defects, the organization of the Golgi network of nev is restored in the evr, serk1, and cst backgrounds. It was concluded that these suppressors act downstream of NEV to spatially inhibit organ separation.…”

“…49 Collectively, both parallel and convergent signaling pathways mediated by NEV-and IDA-HAE/HSL2 modules contribute to floral organ abscission. [9][10][11]44,49 Based on the petal break-strength profiles and the collective observations of uncontrolled cell enlargement and expansion in nev mutants, the role of NEV-mediated intracellular trafficking is required for cell separation (Phase 3), and for organ separation and cell expansion (Phase 4) (Fig. 1B(iii)).…”

“…These include organ fate controlling transcription factors, leucine-rich repeat (LRR) receptor-like kinases, a small signaling peptide, a membrane traffic regulator, MADS-box transcription factors, and central components from several hormone pathways. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] These studies have also uncovered distinct features of the abscission process associated with particular molecular components. Some of these components are considered to be essential for organ separation while others are responsible for controlling the timing of process.…”