![macvector recombination macvector recombination](https://static.cambridge.org/binary/version/id/urn:cambridge.org:id:binary-alt:20170811104548-16882-optimisedImage-S0967199415000374_fig5g.jpg)
Inactivation of Poln in mouse embryonic fibroblasts did not alter cellular sensitivity to mitomycin C, cisplatin, or aldehydes. We examined the response to DNA crosslinking agents, as purified pol ν has some ability to bypass major groove peptide adducts and residues of DNA crosslink repair.
![macvector recombination macvector recombination](https://media.springernature.com/full/springer-static/image/art:10.1186%2F1471-2180-12-118/MediaObjects/12866_2012_Article_1811_Fig4_HTML.jpg)
Pol ν-defective mice had no alteration in DNA end-joining during immunoglobulin class-switching, in contrast to animals defective in the related DNA polymerase θ (pol θ). These polymorphisms are suggested to generate a looped-out primer and a hairpin structure during recombination, substrates on which pol ν can operate. However, pol ν–disrupted mice have a modestly reduced crossover frequency at a meiotic recombination hot spot harboring insertion/deletion polymorphisms. Mice with inactive Poln are fertile and have normal testis morphology. We constructed multiple mouse models for Poln disruption and detected no anatomic abnormalities, alterations in lifespan, or changed causes of mortality. POLN is very weakly expressed in most tissues, with the highest relative expression in testis. Here we report an in-depth analysis of pol ν–defective mice and human cells. DNA polymerase ν (pol ν), encoded by the POLN gene, is an A-family DNA polymerase in vertebrates and some other animal lineages.