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397 A GPI-Anchored Protein Regulates Stimulus-Induced Root Hair Elongation<br />

Yoshihiro Koshino-Kimura 1 , Haruna Kiriyama 1 , Akira Yoshimori 1 , Miyuki Kubo 1 , Takuji Wada 2 , Taisuke Nishimura 3 ,<br />

Mayumi Ohta 1 , Sumie Ishiguro 4 , Ryuji Tsugeki 1 , Noritaka Matsumoto 1 , Kiyotaka Okada 1<br />

1<br />

Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan, 2 Plant Science Center, RIKEN,<br />

Yokohama 230-0045, Japan, 3 Laboratory of Plant Genetics, University of Geneva, Geneva, Switzerland,<br />

4<br />

Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya 464-8601, Japan<br />

To uptake water and nutrients efficiently, plants have many root hairs on their roots. In order to fulfill their function,<br />

roots and root hairs should touch soil. Length and direction of Arabidopsis root hairs are changed depending on touch<br />

or untouch of the root tip to agar surface. When roots are grown on agar surface, root hairs are perpendicular to the root<br />

surface, however, when roots come apart from the agar, hairs get longer and tilted to the root tip. To clarify the molecular<br />

mechanism of this response, we isolated mutants defective in this response. Root hairs of timid (tmd) mutant are shorter<br />

on agar than those of wild type, and become still much shorter when the root does not touch agar. The direction of the<br />

root hairs in tmd were, however, normally changed when the root came off the agar surface. Map-based cloning revealed<br />

that the TMD gene encodes a putative GPI-anchored protein. The TMD gene began to be expressed in hair-forming cells<br />

just before the root-hair bulge were observed. The TMD protein was shown to be localized in plasma membranes and<br />

endosomes. Possible function of TMD protein in the elongation of root hairs in response to the environment will be<br />

discussed.<br />

398 Isolation and Characterization of SOR12, a Novel Regulator of Cytokinin-Mediated Leaf<br />

Senescence<br />

In Chul Lee, Hyo Jung Kim, Tae Hoon Kim, Seung Hee Choi, Hong Gil Nam<br />

Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, Kyungbuk,<br />

790-784, Korea<br />

Senescence is a sequence of biochemical and physiological events that constitute the final stage of development.<br />

Senescence is now clearly regarded as a genetically programmed and evolutionally acquired developmental process.<br />

However, in spite of the biological and practical importance, genetic mechanism of senescence has been very limited.<br />

Previously, we reported that ore12-1 has increased leaf longevity due to a missense mutation in AHK3, a sensor<br />

histidine kinase cytokinin receptor, and suggested that cytokinins exert their anti-senescing effect specifically and<br />

positively through AHK3 to control senescence (Kim et al., 2006). To identify signaling components downstream of<br />

AHK3, we have undertaken a systematic genetic screening in an ore12-1 allele through ethyl methanesulfonate (EMS)-<br />

mutagenesis. One suppressor named sor12 (suppressor of ore12-1) was identified and showed complete suppression of<br />

the ore12-1 senescence phenotypes. sor12 ore12-1 double mutants exhibited accelerated senescence symptoms in agedependent<br />

leaf senescence as well as in dark-induced senescence. Furthermore, sor12 ore12-1 dramatically reduced the<br />

sensitivity of the plant to cytokinins in delaying leaf senescence and in inducing cytokinin-responsive genes, although<br />

these mutants still showed normal sensitivity to cytokinins in other responses, such as shoot induction and hypocotyl<br />

elongation inhibition.<br />

Therefore, we suggest that SOR12 plays a major role in controlling cytokinin-mediated leaf senescence as a<br />

downstream component of AHK3. The identification of the mutated genes is underway and will be reported soon.

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