Equal Sister Chromatid Exchange Is a Major Mechanism of Double-Strand Break Repair in Yeast

Equal sister chromatid exchange (SCE) has been thought to be an important mechanism of double-strand break (DSB) repair in eukaryotes, but this has never been proven due to the difficulty of distinguishing SCE products from parental molecules. To evaluate the biological relevance of equal SCE in DSB...

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Bibliographic Details
Published in:Molecular cell 2003-06, Vol.11 (6), p.1661-1671
Main Authors: González-Barrera, Sergio, Cortés-Ledesma, Felipe, Wellinger, Ralf E, Aguilera, Andrés
Format: Article
Language:English
Subjects:
Chromatids - drug effects
Deoxyribonucleases, Type II Site-Specific - pharmacology
DNA Damage - genetics
DNA Repair - genetics
DNA, Fungal - drug effects
DNA, Fungal - genetics
DNA, Fungal - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Endodeoxyribonucleases - genetics
Endodeoxyribonucleases - metabolism
Exodeoxyribonucleases - genetics
Exodeoxyribonucleases - metabolism
Fungal Proteins - genetics
Fungal Proteins - metabolism
Gene Conversion - drug effects
Kinetics
Mitosis - genetics
Models, Genetic
Rad51 Recombinase
Recombination, Genetic
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - metabolism
Sister Chromatid Exchange
Substrate Specificity
Templates, Genetic
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Summary:Equal sister chromatid exchange (SCE) has been thought to be an important mechanism of double-strand break (DSB) repair in eukaryotes, but this has never been proven due to the difficulty of distinguishing SCE products from parental molecules. To evaluate the biological relevance of equal SCE in DSB repair and to understand the underlying molecular mechanism, we developed recombination substrates for the analysis of DSB repair by SCE in yeast. In these substrates, most breaks are limited to one chromatid, allowing the intact sister chromatid to serve as the repair template; both equal and unequal SCE can be detected. We show that equal SCE is a major mechanism of DSB repair, is Rad51 dependent, and is stimulated by Rad59 and Mre11. Our work provides a physical analysis of mitotically occurring SCE in vivo and opens new perspectives for the study and understanding of DSB repair in eukaryotes.
ISSN:1097-2765
1097-4164
DOI:10.1016/S1097-2765(03)00183-7