Journal
PHOTOCHEMISTRY AND PHOTOBIOLOGY
Volume -, Issue -, Pages -Publisher
WILEY
DOI: 10.1111/php.13879
Keywords
DNA replication; lesion bypass; polymerase eta; polymerase iota; pyrimidine dimers; translesion synthesis; ultraviolet light
Categories
Ask authors/readers for more resources
Xeroderma pigmentosum (XP) variant cells deficient in Polη polymerase show increased sensitivity to UV radiation, affecting cell proliferation and migration. Polι may act as a backup for Polη in bypassing UV-induced photoproducts.
Xeroderma pigmentosum (XP) variant cells are deficient in the translesion synthesis (TLS) DNA polymerase Pol eta (eta). This protein contributes to DNA damage tolerance, bypassing unrepaired UV photoproducts and allowing S-phase progression with minimal delay. In the absence of Pol eta, backup polymerases perform TLS of UV lesions. However, which polymerase plays this role in human cells remains an open question. Here, we investigated the potential role of Pol iota (iota) in bypassing ultraviolet (UV) induced photoproducts in the absence of Pol eta, using NER-deficient (XP-C) cells knocked down for Pol iota and/or Pol eta genes. Our results indicate that cells lacking either Pol iota or Pol eta have increased sensitivity to UVC radiation. The lack of both TLS polymerases led to increased cell death and defects in proliferation and migration. Loss of both polymerases induces a significant replication fork arrest and G1/S-phase blockage, compared to the lack of Pol eta alone. In conclusion, we propose that Pol iota acts as a bona fide backup for Pol eta in the TLS of UV-photoproducts.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available