The stalling of transcription at abasic sites is highly mutagenic

Sung Lim Yu, Sung Keun Lee, Robert E. Johnson, Louise Prakash, Satya Prakash

Research output: Contribution to journalArticle

84 Citations (Scopus)

Abstract

Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.

Original languageEnglish (US)
Pages (from-to)382-388
Number of pages7
JournalMolecular and Cellular Biology
Volume23
Issue number1
DOIs
StatePublished - Jan 2003

Fingerprint

Cockayne Syndrome
RNA Polymerase II
DNA
Mutagenesis
Genes
Saccharomyces cerevisiae

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

The stalling of transcription at abasic sites is highly mutagenic. / Yu, Sung Lim; Lee, Sung Keun; Johnson, Robert E.; Prakash, Louise; Prakash, Satya.

In: Molecular and Cellular Biology, Vol. 23, No. 1, 01.2003, p. 382-388.

Research output: Contribution to journalArticle

Yu, Sung Lim ; Lee, Sung Keun ; Johnson, Robert E. ; Prakash, Louise ; Prakash, Satya. / The stalling of transcription at abasic sites is highly mutagenic. In: Molecular and Cellular Biology. 2003 ; Vol. 23, No. 1. pp. 382-388.
@article{c07230b48d294870b191ba568b36ea29,
title = "The stalling of transcription at abasic sites is highly mutagenic",
abstract = "Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.",
author = "Yu, {Sung Lim} and Lee, {Sung Keun} and Johnson, {Robert E.} and Louise Prakash and Satya Prakash",
year = "2003",
month = "1",
doi = "10.1128/MCB.23.1.382-388.2003",
language = "English (US)",
volume = "23",
pages = "382--388",
journal = "Molecular and Cellular Biology",
issn = "0270-7306",
publisher = "American Society for Microbiology",
number = "1",

}

TY - JOUR

T1 - The stalling of transcription at abasic sites is highly mutagenic

AU - Yu, Sung Lim

AU - Lee, Sung Keun

AU - Johnson, Robert E.

AU - Prakash, Louise

AU - Prakash, Satya

PY - 2003/1

Y1 - 2003/1

N2 - Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.

AB - Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.

UR - http://www.scopus.com/inward/record.url?scp=0037215540&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037215540&partnerID=8YFLogxK

U2 - 10.1128/MCB.23.1.382-388.2003

DO - 10.1128/MCB.23.1.382-388.2003

M3 - Article

C2 - 12482989

AN - SCOPUS:0037215540

VL - 23

SP - 382

EP - 388

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

SN - 0270-7306

IS - 1

ER -