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First published online February 20, 2009
doi: 10.1242/10.1242/dev.030585

Development 136, 1039-1048 (2009)
Published by The Company of Biologists 2009
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Jasmonic acid control of GLABRA3 links inducible defense and trichome patterning in Arabidopsis

Yuki Yoshida1,2, Ryosuke Sano3, Takuji Wada3, Junji Takabayashi2 and Kiyotaka Okada1,4,*

1 Department of Botany, Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan.
2 Center for Ecological Research, Kyoto University, Otsu 520-2113, Japan.
3 Plant Science Center, RIKEN, Yokohama 230-0045, Japan.
4 National Institute for Basic Biology, Okazaki 444-8585, Japan.

* Author for correspondence (e-mail: kiyo{at}nibb.ac.jp)

Accepted 26 January 2009

Once attacked by herbivores, plants regenerate new leaves with increased trichome density as an inducible defense. Trichomes are specified from neighboring epidermal cells through local cell-cell interactions in the leaf primordia. However, the molecular mechanism of how herbivore-induced damage at older leaves remodels the pattern of trichome fate specification at newly forming leaves is largely unknown. In this study, we show that mutations in either the biosynthetic or signaling pathway of jasmonates (JAs), long-distance wound signals, abolish the wound-induced formation of trichomes. To identify the factors linking JA signaling to trichome fate specification, we isolated a novel class of mutants, unarmed (urm), which lack trichome induction but show otherwise normal responses to JAs. URM9 encodes an Importin β family protein, and URM23 is identical to TRANSPARENT TESTA GLABRA1 (TTG1), the product of which interacts with the bHLH transcription factor GLABRA3 (GL3). Loss of either URM9 or URM23 disrupts the subnuclear localization of GL3, thus implicating GL3 in trichome induction. The expression of GL3 was enhanced by JA treatment prior to trichome initiation. Genetic analysis of multiple trichome mutants shows that GL3, in concert with the R2R3-Myb transcription factor GLABRA1 (GL1), promotes trichome fate in response to JA in a dosage-dependent manner. These results indicate that GL3 is a key transcription factor of wound-induced trichome formation acting downstream of JA signaling in Arabidopsis.

Key words: Pattern formation, Cell fate, Plasticity, Trichome, Inducible defense, Jasmonate, Importin β, Arabidopsis thaliana, GLABRA3


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