The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability

Farjana J. Fattah, Kodai Hara, Kazi R. Fattah, Chenyi Yang, Nan Wu, Ross Warrington, David J. Chen, Pengbo Zhou, David A. Boothman, Hongtao Yu

Research output: Contribution to journalArticle

22 Citations (Scopus)

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.

Original languageEnglish (US)
Article numbere1004419
JournalPLoS Genetics
Volume10
Issue number6
DOIs
StatePublished - 2014

Fingerprint

TFII Transcription Factors
Genomic Instability
Proliferating Cell Nuclear Antigen
genomics
transcription factors
DNA
DNA Damage
synthesis
Williams Syndrome
tolerance
DNA Replication
damage
Catalytic Domain
DNA damage
Nucleotides
lesion
sliding
DNA replication
protein subunits
lesions (animal)

ASJC Scopus subject areas

  • Genetics
  • Molecular Biology
  • Ecology, Evolution, Behavior and Systematics
  • Cancer Research
  • Genetics(clinical)

Cite this

The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability. / Fattah, Farjana J.; Hara, Kodai; Fattah, Kazi R.; Yang, Chenyi; Wu, Nan; Warrington, Ross; Chen, David J.; Zhou, Pengbo; Boothman, David A.; Yu, Hongtao.

In: PLoS Genetics, Vol. 10, No. 6, e1004419, 2014.

Research output: Contribution to journalArticle

Fattah, FJ, Hara, K, Fattah, KR, Yang, C, Wu, N, Warrington, R, Chen, DJ, Zhou, P, Boothman, DA & Yu, H 2014, 'The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability', PLoS Genetics, vol. 10, no. 6, e1004419. https://doi.org/10.1371/journal.pgen.1004419
Fattah, Farjana J. ; Hara, Kodai ; Fattah, Kazi R. ; Yang, Chenyi ; Wu, Nan ; Warrington, Ross ; Chen, David J. ; Zhou, Pengbo ; Boothman, David A. ; Yu, Hongtao. / The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability. In: PLoS Genetics. 2014 ; Vol. 10, No. 6.
@article{371af6cf94a3468ab00fc5c92d97545b,
title = "The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability",
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.",
author = "Fattah, {Farjana J.} and Kodai Hara and Fattah, {Kazi R.} and Chenyi Yang and Nan Wu and Ross Warrington and Chen, {David J.} and Pengbo Zhou and Boothman, {David A.} and Hongtao Yu",
year = "2014",
doi = "10.1371/journal.pgen.1004419",
language = "English (US)",
volume = "10",
journal = "PLoS Genetics",
issn = "1553-7390",
publisher = "Public Library of Science",
number = "6",

}

TY - JOUR

T1 - The Transcription Factor TFII-I Promotes DNA Translesion Synthesis and Genomic Stability

AU - Fattah, Farjana J.

AU - Hara, Kodai

AU - Fattah, Kazi R.

AU - Yang, Chenyi

AU - Wu, Nan

AU - Warrington, Ross

AU - Chen, David J.

AU - Zhou, Pengbo

AU - Boothman, David A.

AU - Yu, Hongtao

PY - 2014

Y1 - 2014

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84903487047&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84903487047&partnerID=8YFLogxK

U2 - 10.1371/journal.pgen.1004419

DO - 10.1371/journal.pgen.1004419

M3 - Article

C2 - 24922507

AN - SCOPUS:84903487047

VL - 10

JO - PLoS Genetics

JF - PLoS Genetics

SN - 1553-7390

IS - 6

M1 - e1004419

ER -