| First Author | Parlanti E | Year | 2004 |
| Journal | DNA Repair (Amst) | Volume | 3 |
| Issue | 7 | Pages | 703-10 |
| PubMed ID | 15177179 | Mgi Jnum | J:91067 |
| Mgi Id | MGI:3045901 | Doi | 10.1016/j.dnarep.2003.12.009 |
| Citation | Parlanti E, et al. (2004) Aphidicolin-resistant and -sensitive base excision repair in wild-type and DNA polymerase beta-defective mouse cells. DNA Repair (Amst) 3(7):703-10 |
| abstractText | Several DNA polymerases (Pols) can add complementary bases at the gap created during the base excision repair (BER). To characterize the BER resynthesis step, the repair of a single abasic site by wild-type and Pol beta-defective mouse cell extracts was analysed in the presence of aphidicolin, a specific inhibitor of replicative Pols. We show that there is a competition between distributive and processive Pols for the nucleotide addition at the primer terminus. In wild-type cell extracts, the initial nucleotide insertion involves mainly Pol beta but the elongation step is carried out by a replicative Pol. Conversely, in Pol beta-null cell extracts the synthesis step is carried out by a replicative Pol without any switching to an auxiliary polymerase. We present evidence that short-patch repair synthesis occurs even in the absence of both Pol beta and replicative Pols. Exogeneously added purified human Pol lambda was unable to stimulate this back-up synthesis. |
