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75 Integrating Membrane Transport with Male Gametophyte ... - TAIR

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229 Wound-Inducible Upregulation of Trichome Density is Dependent on Jasmonic Acid<br />

Signaling<br />

Yuki Yoshida 1 , Junji Takabayashi 2<br />

1<br />

Graduate School of Science, Kyoto University, 2 Center for Ecological Research, Kyoto University<br />

Spacing of trichomes is important for their functions, one of which is a structural barrier against herbivores. Molecular<br />

genetic studies have revealed that a family of small MYB proteins, including TRIPTYCHON (TRY) and CAPRICE<br />

(CPC), plays a critical role in lateral-inhibition-based patterning of trichomes. Despite the importance of TRY/CPC, it has<br />

been suggested that there are still other unknown pathways to regulate trichome density. We aimed to gain insight into<br />

such novel aspects of trichome patterning. We focused on the wound-inducible upregulation of trichome density, which<br />

was recently reported by Traw and Bergelson (2003). Plastic change in trichome density is observed also in various plant<br />

species other than Arabidopsis, and is generally considered to be an induced defense against herbivory.<br />

Here we show that allene oxide synthase (aos) mutant, defective in jasmonic acid biosynthesis, failed to upregulate<br />

their trichome density when wounded. In normal growth condition, aos mutant produced trichomes comparable to wild<br />

type. CORONATINE INSENSITIVE1 (COI1) encodes an F-box protein essential for jasmonic acid signaling. Like aos<br />

mutant, coi1-1 mutant also failed to increase their trichomes when wounded. These results indicated that both biosynthesis<br />

and SCF COI1 -complex-mediated signaling of jasmonic acid are essential for the regulation of trichome density in response<br />

to wounding, though not required for the normal differentiation of trichome cells. In contrast, other mutants <strong>with</strong> altered<br />

response to jasmonic acid, namely jasmonate insensitive1-7 (jin1-7) and jasmonate resistant1-1 (jar1-1), did not show<br />

any defects in the wound-responsive upregulation of trichome density, indicating that JIN1 and JAR1 are not required<br />

for the jasmonic acid signaling involved in the regulation of trichome density.<br />

Interestingly, try-29760 and cpc-2 mutants, defective in the lateral inhibition of trichomes, were able to upregulate<br />

their trichome density when treated <strong>with</strong> jasmonic acid. This raised the possibility that the effect of jasmonic acid on<br />

trichome patterning acts independently from TRY/CPC. Currently, we are further investigating the relationship of jasmonic<br />

acid signaling <strong>with</strong> TRY/CPC dependent pathway of epidermal pattern formation.<br />

Traw and Bergelson, Plant Physiology 133: 1367-13<strong>75</strong> (2003)<br />

230 Studies of Auxin Inducible Genes in Association <strong>with</strong> Early Transdifferentiation Process into<br />

Tracheary Elements Using cDNA Microarray<br />

Saiko Yoshida 1 , Taku Demura 2 , Hiroo Fukuda 1<br />

1<br />

Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 2 Plant Science<br />

Center, RIKEN<br />

Apical-basal polar auxin transport is believed to function in the formation of a continuous vascular strand. Polar<br />

auxin transport inhibitors cause ectopic vascular formation at leaf margins and parallel vascular strands at the central<br />

regions. We previously founded that an auxin transport inhibitor, NPA prevented tracheary element (TE) differentiation<br />

from isolated Zinnia mesophyll cells and auxin overcame its prevention. Furthermore, detailed analysis showed that<br />

intracellular free NAA was decreased by the treatment of NPA (Yoshida et al., Plant and Cell Physiology, 46, 2019-28,<br />

2005). It suggested that NPA prevented TE differentiation by decrease of active form of NAA, and the addition of excess<br />

amount of NAA may compensate this depletion. In this study, we performed microarray analysis of genes expressed in<br />

NPA-treated cells and NPA plus NAA-treated cells, to get an insight into auxin regulations of transdifferentiation. The<br />

systematic gene expression analysis revealed that NAA suppressed the expression of wound response genes and promotes<br />

the expression of early xylogenesis/procambium formation-related genes. NAA promoted the expression of Arabidopsis<br />

gene homologues related to auxin signaling, auxin influx, hormone biosynthesis, hormone metabolism, transcription<br />

and transport at early stage of transdifferentiation. Based on these results, auxin action at the transdifferentiation into<br />

tracheary elements is discussed.

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