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ERECTA-family genes coordinate stem cell functions between the epidermal and internal layers of the shoot apical meristem.

Authors
  • Kimura, Yuka1, 2
  • Tasaka, Masao3
  • Torii, Keiko U4, 2, 5, 6
  • Uchida, Naoyuki4, 2
  • 1 Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan. , (Japan)
  • 2 Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8602, Japan. , (Japan)
  • 3 Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, 630-0192, Japan. , (Japan)
  • 4 Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan [email protected] [email protected] , (China)
  • 5 Department of Biology, University of Washington, Seattle, WA 98195, USA.
  • 6 Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.
Type
Published Article
Journal
Development
Publisher
The Company of Biologists
Publication Date
Jan 08, 2018
Volume
145
Issue
1
Identifiers
DOI: 10.1242/dev.156380
PMID: 29217754
Source
Medline
Keywords
License
Unknown

Abstract

The epidermal cell layer and the tissues that lie underneath have different intrinsic functions during plant development. The stem cells within the shoot apical meristem (SAM) that give rise to aerial structures are located in the epidermal and internal tissue layers. However, our understanding of how the functions of these stem cells are coordinated across tissue layers so stem cells can behave as a single population remains limited. WUSCHEL (WUS) functions as a master regulator of stem cell activity. Here, we show that loss of function in the ERECTA (ER)-family receptor kinase genes can rescue the mutant phenotype of wus plants (loss of stem cells), as demonstrated by the reinstated expression of a stem cell marker gene in the SAM epidermis. Localized ER expression in the epidermis can suppress the SAM phenotype caused by loss of ER-family activity. Furthermore, the CLAVATA3- and cytokinin-induced outputs, which contribute to stem cell homeostasis, are dysfunctional in a tissue layer-specific manner in ER-family mutants. Collectively, our findings suggest that the ER family plays a role in the coordination of stem cell behavior between different SAM tissue layers.

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