Signaling in the Arabidopsis shoot meristem stem cell niche correlates with ligand-dependent trafficking of the CLV1 receptor kinase

Cell numbers in above-ground meristem types of plants are thought to be maintained by a feedback loop driven by perception of the glycopeptide ligand CLAVATA3 (CLV3) by the CLAVATA1 (CLV1) receptor kinase and the CLV2/CORYNE (CRN) receptor-like complex [1]. CLV3 made in the stem cells at the meristem apex limits the expression level of the stem cellpromoting homeodomain protein WUSCHEL (WUS) in the cells beneath, where CLV1 as well as WUS RNA are localized. WUS downregulation nonautonomously reduces stem cell proliferation. High-level overexpression of CLV3 eliminates the stem cells and causes meristem termination [2], and loss of CLV3 function allows meristem overproliferation [3]. There are many open questions regarding the CLV3/CLV1 interaction, including where in the meristem it occurs, how it is regulated, and how it is that a large range of CLV3 concentrations gives no meristem size phenotype [4]. Here we use genetics and live imaging to examine the cell biology of CLV1 in Arabidopsis meristematic tissue. We demonstrate that plasma membrane-localized CLV1 is reduced in concentration by CLV3, which causes trafficking of CLV1 to lytic vacuoles. We find that changes in CLV2 activity have no detectable effects on CLV1 levels. We also find that CLV3 appears to diffuse broadly in meristems, contrary to a recent sequestration model which states that CLV3 is quantitatively bound by CLV1 in the apical regions of the meristem, allowing continued WUS activity in lower regions [5]. This study provides a new model for CLV1 function in plant stem cell maintenance and suggests that downregulation of plasma membrane-localized CLV1 by its CLV3 ligand can account for the buffering of CLV3 signaling in the maintenance of stem cell pools in plants.