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Published on May 20, 2005; 10.1104/pp.105.060236

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Received January 26, 2005
Returned for revision February 28, 2005
Accepted March 9, 2005

Roles of Arabidopsis AtREV1 and AtREV7 in Translesion Synthesis

Shinya Takahashi *, Ayako Sakamoto , Shusei Sato , Tomohiko Kato , Satoshi Tabata , and Atsushi Tanaka

Department of Ion-beam-applied Biology, Japan Atomic Energy Research Institute, Watanuki 1233, Takasaki, Gunma, 370-1292, Japan
Kazusa DNA Research Institute, 2-6-7, Kazusa-Kamatari, Kisarazu, Chiba, 292-0812, Japan

* Corresponding author; email: staka{at}taka.jaeri.go.jp.

Plants have mechanisms for repairing and tolerating detrimental effects by various DNA damaging agents. A tolerance pathway that has been predicted to be present in higher plants is translesion synthesis (TLS), which is catalyzed by polymerases. In Arabidopsis (Arabidopsis thaliana), however, the only gene known to be involved in TLS is the Arabidopsis homolog of REV3, AtREV3, which is a putative catalytic subunit of Arabidopsis DNA polymerase {zeta}. A disrupted mutant of AtREV3, rev3, was previously found to be highly sensitive to ultraviolet-B (UV-B) and various DNA damaging agents. REV1 and REV7 are thought to be components of translesion synthesis in plants. In this study, we identified the Arabidopsis homologs of REV1 and REV7 (AtREV1 and AtREV7). Several mutants carrying disrupted AtREV1 and AtREV7 genes were isolated from Arabidopsis T-DNA-inserted lines. An AtREV1-disrupted mutant, rev1, was found to be moderately sensitive to UV-B and DNA cross-linkers. A rev1rev3 double mutant, like rev3, showed high sensitivity to UV-B, {gamma}-rays, and DNA cross-linkers. An AtREV7-disrupted mutant, rev7, was possibly sensitive to cis-diamminedichloroplatinum(II), a kind of DNA cross-linker, but it was not sensitive to acute UV-B and {gamma}-ray irradiation. On the other hand, the aerial growth of rev7, like the aerial growth of rev1 and rev3, was inhibited by long-term UV-B. These results suggest that a TLS mechanism exists in a higher plant and show that AtREV1 and AtREV7 have important roles in tolerating exposure to DNA-damaging agents.




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