First published online March 22, 2002; 10.1104/pp.010894
Plant Physiol, May 2002, Vol. 129, pp. 64-71
An Ultraviolet-B-Resistant Mutant with Enhanced DNA Repair in
Arabidopsis
Atsushi
Tanaka,*
Ayako
Sakamoto,
Yasuhito
Ishigaki,
Osamu
Nikaido,
Guakin
Sun,
Yoshihiro
Hase,
Naoya
Shikazono,
Shigemitsu
Tano, and
Hiroshi
Watanabe
Department of Radiation Research for Environment and
Resources, Takasaki Radiation Chemistry Research Establishment, Japan
Atomic Energy Research Institute, Watanuki-machi 1233, Takasaki, Gunma
370-1292, Japan (A.T., A.S., G.S., Y.H., N.S., S.T., H.W.); and
Faculty of Pharmaceutical Science, Kanazawa University, Takaramachi
13-1, Kanazawa City, Kanazawa 920-0934, Japan (Y.I., O.N.)
An ultraviolet-B (UV-B)-resistant mutant,
uvi1 (UV-B insensitive 1), of Arabidopsis
was isolated from 1,280 M1 seeds that had
been exposed to ion beam irradiation. The fresh weight of uvi1 under high-UV-B exposure was more than
twice that of the wild type. A root-bending assay indicated that root
growth was less inhibited by UV-B exposure in uvi1 than in
the wild type. When the seedlings were grown under white light, the
UV-B dose required for 50% inhibition was about 6 kJ m 2
for the wild type and 9 kJ m2 for uvi1. When
the seedlings were irradiated with UV-B in darkness, the dose required
for 50% inhibition was about 1.5 kJ m2 for the wild type
and 4 kJ m2 for uvi1. An enzyme-linked
immunosorbent assay showed that the reduction in levels of cyclobutane
pyrimidine dimers (CPDs) under white light and of (6-4) photoproducts
in darkness occurred faster in uvi1 than in the wild type.
These results indicate that uvi1 had increased
photoreactivation of CPDs and dark repair of (6-4) photoproducts,
leading to strong UV-B resistance. Furthermore, the transcript levels
of PHR1 (CPD photolyase gene) were much higher in
uvi1 than in the wild type both under white light and after
UV-B exposure. Placing the plants in the dark before UV-B exposure
decreases the early reduction of CPDs in the wild type but not in
uvi1. Our results suggest that UVI1 is a negative
regulator of two independent DNA repair systems.
*
Corresponding author; e-mail atanaka{at}taka.jaeri.go.jp; fax
81-27-346-9688.
© 2002 American Society of Plant Physiologists
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