TPLATE complex dependent endocytosis is required for shoot apical meristem maintenance by attenuating CLAVATA1 signaling

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Wang, Jie | Jiang, Qihang | Pleskot, Roman | Grones, Peter | Denay, Grégoire | Galván-Ampudia, Carlos | Bahafid, Elmehdi | Xu, Xiangyu | Vandorpe, Michael | Mylle, Evelien | de Smet, Ive | Vernoux, Teva | Simon, Rüdiger | Nowack, Moritz, K | van Damme, Daniel

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Abstract Endocytosis regulates the turnover of cell surface localized receptors, which are crucial for plants to sense and rapidly respond to both endogenous and environmental stimuli. The evolutionarily ancient TPLATE complex (TPC) plays an essential role in clathrin-mediated endocytosis (CME) in Arabidopsis plants. Knockout or strong knockdown of single TPC subunits causes male sterility and seedling lethality phenotypes, complicating analysis of the roles of TPC during plant development. Partially functional alleles of TPC subunits however only cause very mild developmental deviations. Here, we took advantage of the recently reported partially functional TPLATE allele, WDXM2, to investigate a role for TPC-dependent endocytosis in receptor-mediated signalling. We discovered that reduced TPC-dependent endocytosis confers a hypersensitivity to very low doses of CLAVATA3 (CLV3) peptide signalling. This hypersensitivity correlated with the abundance of the CLV3 receptor protein kinase CLAVATA1 (CLV1) at the plasma membrane. Genetic analysis and live-cell imaging revealed that TPC-dependent regulation of CLV3-dependent internalization of CLV1 from the plasma membrane is required for CLV3 function in the shoot. Our findings provide evidence that clathrin-mediated endocytosis of CLV1 is a mechanism to dampen CLV3-mediated signaling during plant development.

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