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Mechanisms for Translesion DNA Synthesis
Author(s) -
Yang Wei,
Lee YoungSam,
Gao Yang,
Gregory Mark
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.108.1
Subject(s) - dna polymerase , xeroderma pigmentosum , dna polymerase ii , dna polymerase mu , biology , dna replication , dna synthesis , primer (cosmetics) , dna repair , dna , dna damage , polymerase , dna clamp , genetics , microbiology and biotechnology , chemistry , circular bacterial chromosome , gene , reverse transcriptase , polymerase chain reaction , organic chemistry
In humans among the 17 DNA polymerases identified only five are dedicated to normal DNA replication, and more than 12 are specialized DNA polymerases that are involved in repair and translesion DNA synthesis (TLS). The specialized DNA polymerases are mainly belong to the X and Y families, but a few are in the A and B families and homologous to high‐fidelity replicases. In this talk, I will give examples of DNA polymerases in different structural families that bypass DNA lesions by different mechanisms. For example, human DNA pol eta is essential for UV survival. Deficiency of DNA pol h causes the variant form of Xeroderma Pigmentosum (XPV), characterized by sunlight‐induced pigmentation changes and a highly elevated incidence of skin malignancies. DNA pol z is a B‐family member like E. coli DNA pol II, but it is essential for primer extension in translesion synthesis of a variety of DNA lesions. DNA pol n is an A‐family member and another TLS polymerase. These specialized polymerases appear to use different mechanisms to avoid “road blocks” and carry out translesion DNA synthesis. I will present our most recent results on discerning different mechanisms of TLS essential for cell survival.