| First Author | Ito W | Year | 2012 |
| Journal | Genes Cells | Volume | 17 |
| Issue | 2 | Pages | 98-108 |
| PubMed ID | 22244149 | Mgi Jnum | J:203607 |
| Mgi Id | MGI:5527520 | Doi | 10.1111/j.1365-2443.2011.01576.x |
| Citation | Ito W, et al. (2012) Stalled Poleta at its cognate substrate initiates an alternative translesion synthesis pathway via interaction with REV1. Genes Cells 17(2):98-108 |
| abstractText | DNA polymerase eta (Poleta), whose gene mutation is responsible for the inherited disorder xeroderma pigmentosum variant (XP-V), carries out accurate and efficient translesion synthesis (TLS) across cyclobutane pyrimidine dimer (CPD). As Poleta interacts with REV1, and REV1 interacts with other TLS polymerases including Poliota, Polkappa and Polzeta, Poleta may play a role in recruitment of these TLS polymerases at lesion site. But it is unclear whether UV sensitivity of XP-V patients is caused not only by defect of Poleta activity but also by dysfunction of network between Poleta and other TLS polymerases. Here, we examined whether the TLS polymerase network via Poleta is important for replicative bypass of CPDs and DNA damage tolerance induced by UV in mouse cells. We observed that UV sensitivity of Poleta-deficient mouse cells was moderately rescued by the expression of a catalytically inactive Poleta. Moreover, this recovery of cellular UV sensitivity was mediated by the interaction between Poleta and REV1. However, expression of the inactive mutant Poleta was not able to suppress the incidence of UV-induced mutation observed in Poleta-deficient cells. We propose the model that REV1 and Polkappa are involved in DNA damage tolerance via Poleta-REV1 interaction when Poleta fails to bypass its cognate substrates. |
