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First published online October 12, 2007
doi: 10.1242/10.1242/dev.009597

Development 134, 3873-3882 (2007)
Published by The Company of Biologists 2007
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TRICHOMELESS1 regulates trichome patterning by suppressing GLABRA1 in Arabidopsis

Shucai Wang1, Su-Hwan Kwak2, Qingning Zeng1, Brian E. Ellis3, Xiao-Ya Chen4, John Schiefelbein2,* and Jin-Gui Chen1,*

1 Department of Botany, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
2 Department of Molecular, Cell, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
3 Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
4 National Key Laboratory of Plant Molecular Genetics, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China.

* Authors for correspondence (e-mails: schiefel{at}umich.edu; jingui{at}interchange.ubc.ca)

Accepted 14 August 2007

The patterning of epidermal cell types in Arabidopsis is a simple and useful model for studying the molecular basis of cell specification in plants. The distribution of different cell types in the Arabidopsis epidermis is regulated by a lateral inhibition mechanism that relies on interactions between transcription factors. However, it is unclear how temporal- or organ-specific differences in epidermal patterning are achieved. Here we identify TRICHOMELESS1 (TCL1) as a new and major single-repeat MYB-type transcription factor that negatively regulates trichome formation in the inflorescence epidermis. A dominant mutant with elevated expression of TCL1 has a glabrous (trichomeless) phenotype, whereas a loss-of-function mutation in TCL1 uniquely confers ectopic trichome formation on inflorescence stem and pedicels. Genetic analyses demonstrate that TCL1 and CAPRICE work synergistically to regulate trichome patterning on these organs. Interestingly, overexpression of TCL1 specifically suppresses the expression of GLABRA1 (GL1), a crucial component in the trichome initiation complex, whereas loss-of-function of TCL1 enhances GL1 expression. Chromatin immunoprecipitation results show that TCL1 can be recruited to the cis-acting regulatory elements of GL1. These results provide the first molecular and genetic evidence that an R3 MYB may negatively regulate trichome cell specification in a novel manner by directly suppressing the transcription of GL1.

Key words: Lateral inhibition, MYB, Pattern formation, Trichome, TRICHOMELESS1






© The Company of Biologists Ltd 2007