Generation of Signaling Specificity in Arabidopsis by Spatially Restricted Buffering of Ligand–Receptor Interactions[C][W][OA]

Emily B. Abrash,K. Davies,D. Bergmann

Published 2011 in The Plant Cell

ABSTRACT

Through genetic analysis, this work identifies a growth function for a subset of ligands (CHALf) of the EPFL family. The results indicate that different EPFL members modulate discrete functions of the ER receptor family and that EPFLf signal specificity is achieved through spatial restriction of the TMM receptor, which potentiates stomatal EPFL signals and dampens CHALf growth signals. Core signaling pathways function in multiple programs during multicellular development. The mechanisms that compartmentalize pathway function or confer process specificity, however, remain largely unknown. In Arabidopsis thaliana, ERECTA (ER) family receptors have major roles in many growth and cell fate decisions. The ER family acts with receptor TOO MANY MOUTHS (TMM) and several ligands of the EPIDERMAL PATTERNING FACTOR LIKE (EPFL) family, which play distinct yet overlapping roles in patterning of epidermal stomata. Here, our examination of EPFL genes EPFL6/CHALLAH (CHAL), EPFL5/CHALLAH-LIKE1, and EPFL4/CHALLAH-LIKE2 (CLL2) reveals that this family may mediate additional ER-dependent processes. chal cll2 mutants display growth phenotypes characteristic of er mutants, and genetic interactions are consistent with CHAL family molecules acting as ER family ligands. We propose that different classes of EPFL genes regulate different aspects of ER family function and introduce a TMM-based discriminatory mechanism that permits simultaneous, yet compartmentalized and distinct, function of the ER family receptors in growth and epidermal patterning.

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