ArticleeLife2020
The manifold actions of signaling peptides on subcellular dynamics of a receptor specify stomatal cell fate.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Ligand-induced ubiquitination regulates endocytosis and homeostasis of the ERECTA receptor kinase for stomatal development.The New phytologist · 2026Article
- Comparative proteomic profiling of receptor kinase signaling reveals key trafficking components enforcing plant stomatal development.Science advances · 2026Article
- Clathrin-mediated endocytosis of ERECTA family receptors is essential for proper stomatal development inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Comparative Proteomic Profiling of Receptor Kinase Signaling Reveals Key Trafficking Components Enforcing Plant Stomatal Development.bioRxiv : the preprint server for biology · 2025Article
- Chemical inhibition of stomatal differentiation by perturbation of the master-regulatory bHLH heterodimer via an ACT-Like domain.Nature communications · 2024Article
- Membrane-associated NRPM proteins are novel suppressors of stomatal production in Arabidopsis.Current biology : CB · 2024Article
- Asymmetric Evolution of Protein Domains in the Leucine-Rich Repeat Receptor-Like Kinase Family of Plant Signaling Proteins.Molecular biology and evolution · 2023Article
- Chemical synthesis of the EPF-family of plant cysteine-rich proteins and late-stage dye attachment by chemoselective amide-forming ligations.RSC chemical biology · 2022Article
- Arabidopsis ERdj3B coordinates with ERECTA-family receptor kinases to regulate ovule development and the heat stress response.The Plant cell · 2022Article
- The functional specificity of ERECTA-family receptors in Arabidopsis stomatal development is ensured by molecular chaperones in the endoplasmic reticulum.Development (Cambridge, England) · 2022Article
- Differential regulation of flower transpiration during abiotic stress in annual plants.The New phytologist · 2022Article
- Connected function of PRAF/RLD and GNOM in membrane trafficking controls intrinsic cell polarity in plants.Nature communications · 2022Article
- Stomatal development in the context of epidermal tissues.Annals of botany · 2021Review
- Shouting out loud: signaling modules in the regulation of stomatal development.Plant physiology · 2021Review
- Stomatal Lineage Control by Developmental Program and Environmental Cues.Frontiers in plant science · 2021Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Receptor endocytosis is important for signal activation, transduction, and deactivation. However, how a receptor interprets conflicting signals to adjust cellular output is not clearly understood. Using genetic, cell biological, and pharmacological approaches, we report here that ERECTA-LIKE1 (ERL1), the major receptor restricting plant stomatal differentiation, undergoes dynamic subcellular behaviors in response to different EPIDERMAL PATTERNING FACTOR (EPF) peptides. Activation of ERL1 by EPF1 induces rapid ERL1 internalization via multivesicular bodies/late endosomes to vacuolar degradation, whereas ERL1 constitutively internalizes in the absence of EPF1. The co-receptor, TOO MANY MOUTHS is essential for ERL1 internalization induced by EPF1 but not by EPFL6. The peptide antagonist, Stomagen, triggers retention of ERL1 in the endoplasmic reticulum, likely coupled with reduced endocytosis. In contrast, the dominant-negative ERL1 remained dysfunctional in ligand-induced subcellular trafficking. Our study elucidates that multiple related yet unique peptides specify cell fate by deploying the differential subcellular dynamics of a single receptor.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.