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