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Plant and Cell Physiology Advance Access published online on May 12, 2009
Plant and Cell Physiology, doi:10.1093/pcp/pcp068
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© The Author 2009. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Epidermal cell density is auto-regulated via a secretory peptide, EPIDERMAL PATTERNING FACTOR 2 in Arabidopsis leaves.

Kenta Hara1, Toshiya Yokoo1, Ryoko Kajita1, Takaaki Onishi, Saiko Yahata1, Kylee M. Peterson2, Keiko U. Torii2 and Tatsuo Kakimoto1,*

1 Department of Biological Science, Graduate School of Sciences, Osaka University, Toyonaka, Osaka 560-0043, Japan
2 Department of Biology, University of Washington, Seattle, WA 98195, USA

Corresponding author: Dr. Tatsuo Kakimoto, Department of Biological Sciences, Graduate School of Science, Osaka University. Toyonaka, Osaka 560-0043, Japan. email: kakimoto{at}bio.sci.osaka-u.ac.jp, TEL/FAX: 06-6850-5421


  Abstract

Regulation of the number of cells is critical for development of multicellular organisms. During plant epidermal development, a protodermal cell first makes a fate decision of whether or not to be the meristemoid mother cell (MMC), which undergoes asymmetric cell division forming a meristemoid and its sister cell. The MMC-derived lineage produces all stomatal guard cells and a large proportion of non-guard cells. We demonstrate that a small secretory peptide, EPIDERMAL PATTERING FACTOR 2 (EPF2), is produced by MMC and its early descendants, and negatively regulates the density of guard and non-guard epidermal cells. Our results suggest that EPF2 inhibits cells from adopting the MMC fate in a non-cell-autonomous manner, thus limiting the number of MMCs. This feedback loop is critical for regulation of epidermal cell density. EPF2 resembles in its amino acid sequence to EPF1, which is known to control stomatal positioning. Overexpression of EPF1 also inhibits stomatal development, but EPF1 can act only on a later developmental process than EPF2 can do. Overexpression and promoter-swapping experiments suggested that protein functions of EPF1 and EPF2, rather than expression patterns of these genes, are responsible for the specific functions. Although targets of EPF1 and EPF2 are different, both EPF1 and EPF2 require common putative receptor components TMM, ER, ERL1, and ERL2 to function.

(Received April 27, 2009; Accepted May 7, 2009)
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