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Published on December 23, 2004; 10.1104/pp.104.055145

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Received October 17, 2004
Returned for revision November 4, 2004
Accepted November 8, 2004

The ATE Genes Are Responsible for Repression of Transdifferentiation into Xylem Cells in Arabidopsis

Shinichrio Sawa *, Taku Demura , Gorou Horiguchi , Minoru Kubo , and Hiroo Fukuda

Department of Biological Sciences, Graduate School of Science, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan
Plant Science Center, RIKEN, Yokohama 230-0045, Japan
Department of Biological Sciences, Graduate School of Science, University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan; Plant Science Center, RIKEN, Yokohama 230-0045, Japan

* Corresponding author; email: sawa{at}biol.s.u-tokyo.ac.jp.

We isolated three recessive mutants of Arabidopsis (Arabidopsis thaliana) showing ectopic expression of the xylem-specific marker, pAtxyn3::YFP. Genetic analysis indicated that the phenotypes were caused by mutations in three different genes, designated Abnormal Tracheary Element formation-related gene expression (ate1-3). The ate1 mutants showed a normal DR5::GUS gene expression pattern, and the ate1 mutation did not affect the abnormal vascular pattern formation in the van3 and pin1 mutants, indicating that the ate1 mutation does not affect the vascular pattern organization governed by auxin. The ate mutants showed ectopic lignin deposition, patterned secondary wall thickenings, and cell death, which are characteristic of mature tracheary elements (TEs) in cells ectopically expressing the pAtxyn3::YFP gene. Ectopic TE formation was rapidly induced in parenchymal tissue of the ate mutants in a TE-inducible system with excised hypocotyl. Furthermore, reverse transcription-polymerase chain reaction experiments showed that the expression of TE formation-related genes is up-regulated in the ate mutants. The ate1 mutation also caused ectopic expression of another xylem-specific marker gene, pAt3g62160::YFP. Overall, our results suggest that the ATE genes are responsible for the in situ repression of transdifferentiation into TEs in Arabidopsis and could be participants in the transdifferentiation-masking system.




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