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The DNA excision repair system of the highly radioresistant bacterium Deinococcus radiodurans is facilitated by the pentose phosphate pathway
Author(s) -
Zhang Y.M.,
Liu J.K.,
Wong T.Y.
Publication year - 2003
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2003.03486.x
Subject(s) - biology , deinococcus radiodurans , dna repair , mutant , nucleotide excision repair , pentose phosphate pathway , dna , microbiology and biotechnology , biochemistry , dna damage , gene , enzyme , glycolysis
Summary Deinococcus radiodurans is highly resistant to radiation and mutagenic chemicals. Mutants defective in the putative glucose‐6‐phosphate dehydrogenase gene ( zwf – ) and the aldolase gene ( fda – ) were generated by homologous recombination. These mutants were used to test the cells’ resistance to agents that cause dimer formation and DNA strand breaks. The zwf – mutants were more sensitive to agents that induce DNA excision repair, such as UV irradiation and H 2 O 2 , but were as resistant to DNA strand break‐causing agents such as methylmethanesulphonic acid (MMS) and mitomycin C (MMC) as the wild‐type cells. Analysis of the cytoplasmic fraction of zwf – cells showed that the concentrations of inosine monophosphate (IMP) and uridine monophosphate (UMP) were only 30% of those found in the wild‐type cells. The fda – mutants were slightly more resistant to UV light and H 2 O 2 . Results suggested that the deinococcal pentose phosphate pathway augmented the DNA excision repair system by providing cells with adequate metabolites for the DNA mismatch repair.