scholarly journals Coordination of DNA Ends During Double-Strand-Break Repair in Bacteriophage T4

Genetics ◽  
2002 ◽  
Vol 162 (3) ◽  
pp. 1019-1030
Author(s):  
Bradley A Stohr ◽  
Kenneth N Kreuzer

Abstract The extensive chromosome replication (ECR) model of double-strand-break repair (DSBR) proposes that each end of a double-strand break (DSB) is repaired independently by initiating extensive semiconservative DNA replication after strand invasion into homologous template DNA. In contrast, several other DSBR models propose that the two ends of a break are repaired in a coordinated manner using a single repair template with only limited DNA synthesis. We have developed plasmid and chromosomal recombinational repair assays to assess coordination of the broken ends during DSBR in bacteriophage T4. Results from the plasmid assay demonstrate that the two ends of a DSB can be repaired independently using homologous regions on two different plasmids and that extensive replication is triggered in the process. These findings are consistent with the ECR model of DSBR. However, results from the chromosomal assay imply that the two ends of a DSB utilize the same homologous repair template even when many potential templates are present, suggesting coordination of the broken ends during chromosomal repair. This result is consistent with several coordinated models of DSBR, including a modified version of the ECR model.

DNA Repair ◽  
2006 ◽  
Vol 5 (7) ◽  
pp. 773-787 ◽  
Author(s):  
Victor P. Shcherbakov ◽  
Lidiya Plugina ◽  
Tamara Shcherbakova ◽  
Svetlana Sizova ◽  
Elena Kudryashova

Genetics ◽  
2013 ◽  
Vol 195 (3) ◽  
pp. 739-755 ◽  
Author(s):  
Joshua R. Almond ◽  
Bradley A. Stohr ◽  
Anil K. Panigrahi ◽  
Dustin W. Albrecht ◽  
Scott W. Nelson ◽  
...  

2000 ◽  
Vol 304 (2) ◽  
pp. 151-164 ◽  
Author(s):  
Michael J McIlwraith ◽  
Eric Van Dyck ◽  
Jean-Yves Masson ◽  
Alicja Z Stasiak ◽  
Andrzej Stasiak ◽  
...  

2008 ◽  
Vol 44 (9) ◽  
pp. 1025-1030 ◽  
Author(s):  
V. P. Shcherbakov ◽  
S. T. Sizova ◽  
T. S. Shcherbakova ◽  
I. E. Granovsky ◽  
K. Yu. Popad’in

Genetics ◽  
1995 ◽  
Vol 139 (3) ◽  
pp. 1189-1199
Author(s):  
G T Milne ◽  
T Ho ◽  
D T Weaver

Abstract RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KlRAD52) and RAD51 (KlRAD51) but failed to suppress either a rad52 delta or a rad51 delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively.


1992 ◽  
Vol 12 (6) ◽  
pp. 2464-2474
Author(s):  
P Hasty ◽  
J Rivera-Pérez ◽  
A Bradley

We have analyzed the gene-targeting frequencies and recombination products generated by a series of vectors which target the hprt locus in embryonic stem cells and found the existence of alternative pathways that depend on the location of the double-strand break within the vector. A double-strand break in the targeting homology was found to increase the targeting frequency compared with a double-strand break at the edge of or outside the target homology; this finding agrees with the double-strand break repair model proposed for Saccharomyces cerevisiae. Although a double-strand break in the homology is important for efficient targeting, observations reported here suggest that the terminal ends are not always directly involved in the initial recombination event. Short terminal heterologous sequences which block the homologous ends of the vector may be incorporated into the target locus. A modification of the double-strand break repair model is described to account for this observation.


1992 ◽  
Vol 12 (6) ◽  
pp. 2464-2474 ◽  
Author(s):  
P Hasty ◽  
J Rivera-Pérez ◽  
A Bradley

We have analyzed the gene-targeting frequencies and recombination products generated by a series of vectors which target the hprt locus in embryonic stem cells and found the existence of alternative pathways that depend on the location of the double-strand break within the vector. A double-strand break in the targeting homology was found to increase the targeting frequency compared with a double-strand break at the edge of or outside the target homology; this finding agrees with the double-strand break repair model proposed for Saccharomyces cerevisiae. Although a double-strand break in the homology is important for efficient targeting, observations reported here suggest that the terminal ends are not always directly involved in the initial recombination event. Short terminal heterologous sequences which block the homologous ends of the vector may be incorporated into the target locus. A modification of the double-strand break repair model is described to account for this observation.


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