| First Author | Kazachenko KY | Year | 2017 |
| Journal | DNA Repair (Amst) | Volume | 50 |
| Pages | 77-82 | PubMed ID | 28077248 |
| Mgi Jnum | J:273998 | Mgi Id | MGI:6295221 |
| Doi | 10.1016/j.dnarep.2017.01.001 | Citation | Kazachenko KY, et al. (2017) Alternative splicing at exon 2 results in the loss of the catalytic activity of mouse DNA polymerase iota in vitro. DNA Repair (Amst) 50:77-82 |
| abstractText | Y-family DNA polymerase iota (Pol iota) possesses both DNA polymerase and dRP lyase activities and was suggested to be involved in DNA translesion synthesis and base excision repair in mammals. The 129 strain of mice and its derivatives have a natural nonsense codon mutation in the second exon of the Pol iota gene resulting in truncation of the Pol iota protein. These mice were widely used as a Pol iota-null model for in vivo studies of the Pol iota function. However whether 129-derived strains of mice are fully deficient in the Pol iota functions was a subject of discussion since Pol iota mRNA undergoes alternative splicing at exon 2. Here we report purification of mouse Pol iota lacking the region encoded by exon 2, which includes several conserved residues involved in catalysis. We show that the deletion abrogates both the DNA polymerase and dRP lyase activities of Pol iota in the presence of either Mg(2+) or Mn(2+) ions. Thus, 129-derived strains of mice express catalytically inactive alternatively spliced Pol iota variant, whose cellular functions, if any exist, remain to be established. |
