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Yoshimura, M.* ; Kohzaki, M.* ; Nakamura, J.* ; Asagoshi, K.* ; Sonoda, E.* ; Hou, E.* ; Prasad, R.* ; Wilson, S.H.* ; Tano, K.* ; Yasui, A.* ; Lan, L.* ; Seki, M.* ; Wood, R.D.* ; Arakawa, H. ; Buerstedde, J.M. ; Hochegger, H.* ; Okada, T.* ; Hiraoka, M.* ; Takeda, S.*

Vertebrate POLQ and POLß cooperate in base excision repair of oxidative DNA damage.

Mol. Cell 24, 115-125 (2006)

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Base excision repair (BER) plays an essential role in protecting cells from mutagenic base damage caused by oxidative stress, hydrolysis, and environmental factors. POLQ is a DNA polymerase, which appears to be involved in translesion DNA synthesis (TLS) past base damage. We disrupted POLQ, and its homologs HEL308 and POLN in chicken DT40 cells, and also created polq/hel308 and polq/poln double mutants. We found that POLQ-deficient mutants exhibit hypersensitivity to oxidative base damage induced by H2O2, but not to UV or cisplatin. Surprisingly, this phenotype was synergistically increased by concomitant deletion of the major BER polymerase, POLβ. Moreover, extracts from a polq null mutant cell line show reduced BER activity, and POLQ, like POLβ, accumulated rapidly at sites of base damage. Accordingly, POLQ and POLβ share an overlapping function in the repair of oxidative base damage. Taken together, these results suggest a role for vertebrate POLQ in BER. © 2006 Elsevier Inc. All rights reserved.

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