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ARS Home » Southeast Area » Raleigh, North Carolina » Plant Science Research » Research » Publications at this Location » Publication #157474
Title: RESPONSES OF DNA REPAIR AND FLAVONOID DEFICIENT ARABIDOPSIS MUTANTS TO SOLAR UV-B RADIATION

Author
item Fiscus, Edwin
item Booker, Fitzgerald
item BRITT, ANNE - UNIVERSITY OF CALIFORNIA

Submitted to: American Society for Photobiology
Publication Type: Proceedings
Publication Acceptance Date: 2/1/2003
Publication Date: 7/7/2003
Citation: Fiscus, E.L., Booker, F.L., Britt, A.B. 2003. Responses of DNA repair and flavonoid deficient Arabidopsis mutants to solar UV-B radiation. American Society for Photobiology.

Interpretive Summary:

Technical Abstract: In order to determine which DNA repair pathways play an important role in plant resistance to solar UV-B, DNA repair-deficient mutants (uvr1, uvr2 and uvr3) and their Landsberg erecta (Ler) progenitor were grown under natural light filtered through UV-B transparent (cellulose diacetate, CD) versus UV-B opaque (polyester or polyvinyl chloride, PVC) filters and compared for a number of growth parameters. The mutants were deficient in cyclobutane pyrimidine dimer (CPD) repair (uvr2), photoreactivation of pyrimidine [6,4] pyrimidinone dimers (6-4 products, uvr3) and the slower but more general process of nucleotide excision repair (uvr1). Plants were treated in temperature-controlled outdoor chambers fitted with either polyester of PVC filters. Growth of every line was inhibited by chambers fitted with CD filters compared with polyester or PVC filters. However, inhibitory effects of solar UV-B were most prominent in the uvr2 line (CPD repair deficient). Overall though, plants completely defective in the repair of CPDs did not die on exposure to solar UV-B radiation suggesting that other protective mechanisms effectively attenuate the UV-B exposure to a non-lethal level. The importance of UV-B absorbing compounds was supported by experiments with a triple mutant line (tt5, uvr1, uvr2) in which the effects of solar UV-B was both quick and lethal. These experiments demonstrate the critical interdependence between DNA repair mechanisms and UV-B screening compounds.