Autocrine regulation of stomatal differentiation potential by EPF1 and ERECTA-LIKE1 ligand-receptor signaling

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Cite this article as: eLife 2017;6:e24102 doi: 10.7554/eLife.24102

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Abstract

Development of stomata, valves on the plant epidermis for optimal gas exchange and water control, is fine-tuned by multiple signaling peptides with unique, overlapping, or antagonistic activities. EPIDERMAL PATTERNING FACTOR1 (EPF1) is a founding member of the secreted peptide ligands enforcing stomatal patterning. Yet, its exact role remains unclear. Here, we report that EPF1 and its primary receptor ERECTA-LIKE1 (ERL1) target MUTE, a transcription factor specifying the proliferation-to-differentiation switch within the stomatal cell lineages. In turn, MUTE directly induces ERL1. The absolute co-expression of ERL1 and MUTE, with the co-presence of EPF1, triggers autocrine inhibition of stomatal fate. During normal stomatal development, this autocrine inhibition prevents extra symmetric divisions of stomatal precursors likely owing to excessive MUTE activity. Our study reveals the unexpected role of self-inhibition as a mechanism for ensuring proper stomatal development and suggests an intricate signal buffering mechanism underlying plant tissue patterning.

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Author details

Xingyun Qi

Howard Hughes Medical Institute, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Soon-Ki Han

Howard Hughes Medical Institute, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Jonathan H Dang

Howard Hughes Medical Institute, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Jacqueline M Garrick

Howard Hughes Medical Institute, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Masaki Ito

Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan

Competing interests
The authors declare that no competing interests exist.
Alexander K Hofstetter

Howard Hughes Medical Institute, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Keiko U Torii

Howard Hughes Medical Institute, University of Washington, Seattle, United States

For correspondence
ktorii@u.washington.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-6168-427X

Funding

Howard Hughes Medical Institute

Keiko U Torii

Gordon and Betty Moore Foundation (GBMF3035)

Keiko U Torii

National Science Foundation (MCB-0855659)

Keiko U Torii

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

Sheila McCormick, University of California-Berkeley, United States

Publication history

Received: December 9, 2016
Accepted: March 6, 2017
Accepted Manuscript published: March 7, 2017 (version 1)
Accepted Manuscript updated: March 14, 2017 (version 2)
Version of Record published: March 20, 2017 (version 3)

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.