|
Originally published In Press as doi:10.1074/jbc.M103588200 on June 4, 2001
J. Biol. Chem., Vol. 276, Issue 34, 31551-31560, August 24, 2001
Recombinational and Mutagenic Repair of Psoralen Interstrand
Cross-links in Saccharomyces cerevisiae*
Ross B.
Greenberg ,
Marie
Alberti§,
John E.
Hearst§,
Mark A.
Chua , and
Wilma A.
Saffran ¶
From the Department of Chemistry and Biochemistry,
Queens College, City University of New York, Flushing, New York 11367 and the § Department of Chemistry, Lawrence Berkeley
National Laboratory, University of California, Berkeley, California
94720
Psoralen photoreacts with DNA to form
interstrand cross-links, which can be repaired by both nonmutagenic
nucleotide excision repair and recombinational repair pathways and by
mutagenic pathways. In the yeast Saccharomyces cerevisiae,
psoralen cross-links are processed by nucleotide excision repair
to form double-strand breaks (DSBs). In yeast, DSBs are repaired
primarily by homologous recombination, predicting that cross-link and
DSB repair should induce similar recombination end points. We
compared psoralen cross-link, psoralen monoadduct, and DSB repair using
plasmid substrates with site-specific lesions and measured the patterns of gene conversion, crossing over, and targeted mutation. Psoralen cross-links induced both recombination and mutations, whereas DSBs
induced only recombination, and monoadducts were neither recombinogenic
nor mutagenic. Although the cross-link- and DSB-induced patterns of
plasmid integration and gene conversion were similar in most respects,
they showed opposite asymmetries in their unidirectional conversion
tracts: primarily upstream from the damage site for cross-links but
downstream for DSBs. Cross-links induced targeted mutations in 5% of
the repaired plasmids; all were base substitutions, primarily T C
transitions. The major pathway of psoralen cross-link repair in
yeast is error-free and involves the formation of DSB intermediates
followed by homologous recombination. A fraction of the cross-links
enter an error-prone pathway, resulting in mutations at the damage site.
*
This work was supported in part by grants from the City
University of New York PSC-CUNY Research Award Program (to W. A. S.), the National Institutes of Health Grants CA42377 (to W. A. S.) and
GM47945 (to J. E. H.), and the Office of Basic Energy Sciences in the
Biological Energy division of the Department of Energy under contract
number DE-AC03-76SF00098 (to J. E. H.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
¶
To whom correspondence should be addressed: Dept. of Chemistry
and Biochemistry, Queens College, City University of New York, 65-30 Kissena Blvd., Flushing, NY 11367. Tel.: 718-997-4195; Fax: 718-997-5531; E-mail: Wilma_Saffran@qc.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

CiteULike Complore Connotea Del.icio.us Digg Reddit Technorati What's this?
This article has been cited by other articles:

|
 |

|
 |
 
A. Pamidi, R. Cardoso, A. Hakem, E. Matysiak-Zablocki, A. Poonepalli, L. Tamblyn, B. Perez-Ordonez, M. P. Hande, O. Sanchez, and R. Hakem
Functional Interplay of p53 and Mus81 in DNA Damage Responses and Cancer
Cancer Res.,
September 15, 2007;
67(18):
8527 - 8535.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
X. Shen, S. Jun, L. E. O'Neal, E. Sonoda, M. Bemark, J. E. Sale, and L. Li
REV3 and REV1 Play Major Roles in Recombination-independent Repair of DNA Interstrand Cross-links Mediated by Monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA)
J. Biol. Chem.,
May 19, 2006;
281(20):
13869 - 13872.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Zhang, R. Kaur, X. Lu, X. Shen, L. Li, and R. J. Legerski
The Pso4 mRNA Splicing and DNA Repair Complex Interacts with WRN for Processing of DNA Interstrand Cross-links
J. Biol. Chem.,
December 9, 2005;
280(49):
40559 - 40567.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
W. A. Saffran, S. Ahmed, S. Bellevue, G. Pereira, T. Patrick, W. Sanchez, S. Thomas, M. Alberti, and J. E. Hearst
DNA Repair Defects Channel Interstrand DNA Cross-links into Alternate Recombinational and Error-prone Repair Pathways
J. Biol. Chem.,
August 27, 2004;
279(35):
36462 - 36469.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Majumdar, N. Puri, B. Cuenoud, F. Natt, P. Martin, A. Khorlin, N. Dyatkina, A. J. George, P. S. Miller, and M. M. Seidman
Cell Cycle Modulation of Gene Targeting by a Triple Helix-forming Oligonucleotide
J. Biol. Chem.,
March 21, 2003;
278(13):
11072 - 11077.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. Sridharan, M. Brown, W. C. Lambert, L. W. McMahon, and M. W. Lambert
Nonerythroid {alpha}II spectrin is required for recruitment of FANCA and XPF to nuclear foci induced by DNA interstrand cross-links
J. Cell Sci.,
March 1, 2003;
116(5):
823 - 835.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
H. Zheng, X. Wang, A. J. Warren, R. J. Legerski, R. S. Nairn, J. W. Hamilton, and L. Li
Nucleotide Excision Repair- and Polymerase {eta}-Mediated Error-Prone Removal of Mitomycin C Interstrand Cross-Links
Mol. Cell. Biol.,
January 15, 2003;
23(2):
754 - 761.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
N. Zhang, X. Lu, X. Zhang, C. A. Peterson, and R. J. Legerski
hMutS{beta} Is Required for the Recognition and Uncoupling of Psoralen Interstrand Cross-Links In Vitro
Mol. Cell. Biol.,
April 1, 2002;
22(7):
2388 - 2397.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
|
Advertisement
Advertisement
|