Title | The transcription factor TFII-I promotes DNA translesion synthesis and genomic stability. |
Publication Type | Journal Article |
Year of Publication | 2014 |
Authors | Fattah FJ, Hara K, Fattah KR, Yang C, Wu N, Warrington R, Chen DJ, Zhou P, Boothman DA, Yu H |
Journal | PLoS Genet |
Volume | 10 |
Issue | 6 |
Pagination | e1004419 |
Date Published | 2014 Jun |
ISSN | 1553-7404 |
Keywords | Cell Line, Tumor, DNA Damage, DNA Repair, DNA Replication, DNA-Binding Proteins, DNA-Directed DNA Polymerase, Genomic Instability, HEK293 Cells, HeLa Cells, Humans, Mad2 Proteins, Nuclear Proteins, Nucleotidyltransferases, Proliferating Cell Nuclear Antigen, Transcription Factors, TFII |
Abstract | Translesion synthesis (TLS) enables DNA replication through damaged bases, increases cellular DNA damage tolerance, and maintains genomic stability. The sliding clamp PCNA and the adaptor polymerase Rev1 coordinate polymerase switching during TLS. The polymerases Pol η, ι, and κ insert nucleotides opposite damaged bases. Pol ζ, consisting of the catalytic subunit Rev3 and the regulatory subunit Rev7, then extends DNA synthesis past the lesion. Here, we show that Rev7 binds to the transcription factor TFII-I in human cells. TFII-I is required for TLS and DNA damage tolerance. The TLS function of TFII-I appears to be independent of its role in transcription, but requires homodimerization and binding to PCNA. We propose that TFII-I bridges PCNA and Pol ζ to promote TLS. Our findings extend the general principle of component sharing among divergent nuclear processes and implicate TLS deficiency as a possible contributing factor in Williams-Beuren syndrome. |
DOI | 10.1371/journal.pgen.1004419 |
Alternate Journal | PLoS Genet |
PubMed ID | 24922507 |
PubMed Central ID | PMC4055408 |
Grant List | CA139217 / CA / NCI NIH HHS / United States |
Related Lab:
Related Faculty:
Pengbo Zhou, Ph.D.