ELUCIDATING THE MECHANISM OF ER-FAMILY RECEPTORS IN REGULATION OF STOMATAL DEVELOPMENT AND SHOOT APICAL MERISTEM

ERECTA-family receptors that contain ERECTA (ER), ERECTA LIKE 1 (ERL1), and ERECTA LIKE 2 (ERL2) are important for diverse developmental processes of Arabidopsis, such as organ elongation, stomatal formation, reproductive development, shoot apical meristem (SAM) maintenance and leaf morphology. The activity of ER-family receptors is regulated by small secretory peptides that belong to the EPIDERMAL PATTERNING FACTOR/ LIKE (EPF/ EPFL) family. There are 11 EPF/ EPFL peptides in Arabidopsis. Over the past years, we have gained a better understanding of how ER-family receptors regulate Arabidopsis development, and which EPF/ EPFL ligands are responsible for triggering ERf signal in which developmental process. However, on the protein level, we still do not know how EPF/ EPFL ligands interact with ER-family receptors and how the receptors identify different ligands. The SAM controls the generation of aboveground organs throughout plant life. The er erl1 erl2 triple mutant has an enlarged SAM and exhibits reduced leaf initiation. How the SAM is regulated by ER-family receptors remains unclear. Work presented in this dissertation includes:1) Crystal structures that show details of interactions between ER-family receptors and EPF/ EPFL ligands. Although EPF1/2 and EPFL4/6 are structurally and functionally different from each other, they interact with ER-family receptors similarly through their conserved N-terminal “GS’ motif and central β-sheet. The binding of EPF1/2 to ER-family receptors requires coreceptor TOO MANY MOUTHS (TMM), whereas the presence of TMM greatly reduces the binding affinity of EPFL4/6 to ER-family receptors. Structural comparison revealed that residues involved in contacts between EPF1/2 and TMM are absent in EPF4/6.2) The negative feedback loop between WUSCHEL (WUS) and CLAVATA 3 (CLV3) plays a crucial role in the SAM maintenance. Our genetic analyses indicated that ER-family receptors prevent SAM expansion via suppressing both WUS and CLV3 expression. Since EPF/ EPFL ligands are expressed at the SAM boundary, it is proposed that ERf signal latitudinally restricts the expression of WUS and CLV3 to the central region of the SAM.