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Links between replication and recomb...

Stohr, Bradley Alden.

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Links between replication and recombinational repair during bacteriophage T4 infection.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Links between replication and recombinational repair during bacteriophage T4 infection./
作者:	Stohr, Bradley Alden.
面頁冊數:	136 p.
附註:	Source: Dissertation Abstracts International, Volume: 63-09, Section: B, page: 4044.
Contained By:	Dissertation Abstracts International63-09B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3063207
ISBN:	0493819630

Links between replication and recombinational repair during bacteriophage T4 infection.
Stohr, Bradley Alden.

Links between replication and recombinational repair during bacteriophage T4 infection. - 136 p.

Source: Dissertation Abstracts International, Volume: 63-09, Section: B, page: 4044.

Thesis (Ph.D.)--Duke University, 2002.

Replication and recombinational repair are tightly intertwined during bacteriophage T4 infection. We have explored the connections between these two processes, focusing on both replication-induced recombinational repair and repair-induced replication.

ISBN: 0493819630Subjects--Topical Terms:

1017730
Biology, Genetics.

Links between replication and recombinational repair during bacteriophage T4 infection.
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245 1 0 $a Links between replication and recombinational repair during bacteriophage T4 infection.
300 $a 136 p.
500 $a Source: Dissertation Abstracts International, Volume: 63-09, Section: B, page: 4044.
500 $a Supervisor: Kenneth N. Kreuzer.
502 $a Thesis (Ph.D.)--Duke University, 2002.
520 $a Replication and recombinational repair are tightly intertwined during bacteriophage T4 infection. We have explored the connections between these two processes, focusing on both replication-induced recombinational repair and repair-induced replication.
520 $a Using a two-plasmid assay, we have obtained evidence that one role of the T4 recombinational repair apparatus is to restart disrupted replication forks. The presence of a T4 origin of replication on one plasmid dramatically increases interplasmid recombination and stimulates replication of a second homologous plasmid. We infer that replication forks initiated on the origin plasmid are sometimes disrupted, leading to increased recombination-dependent replication of the homologous plasmid. This origin-induced recombination can be stimulated further with the antitumor drug <italic>m</italic>-AMSA (4<super> ′</super>-(9-acridinylamino)methanesulphon-<italic>m</italic>-anisidide), which traps the T4 type II topoisomerase in a covalent enzyme-DNA cleavage complex. Genetic analyses demonstrate that interplasmid recombinant formation (with or without <italic>m</italic>-AMSA treatment) is absolutely dependent on the products of genes <italic>32</italic> and <italic>46</italic> and largely dependent on the products of genes <italic>uvsX, uvsY</italic>, and <italic> 49</italic>. Similar genetic requirements are observed for repair of endonuclease-generated double-strand breaks (DSBs), suggesting that the origin-induced recombination occurs through a double-strand break intermediate.
520 $a The extensive chromosome replication (ECR) model of DSB repair (DSBR) proposes that each end of a DSB is repaired independently by initiating semi-conservative DNA replication. In contrast, several other DSBR models propose that the two ends of a break are repaired in a coordinated manner with only limited DNA synthesis. We have developed plasmid and chromosomal recombinational repair assays to assess coordination of the broken ends during DSBR. 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, findings consistent with the ECR model of DSBR. However, results from the chromosomal assay suggest 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.
590 $a School code: 0066.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Microbiology. $3 1017734
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710 2 0 $a Duke University. $3 569686
773 0 $t Dissertation Abstracts International $g 63-09B.
790 $a 0066
790 1 0 $a Kreuzer, Kenneth N., $e advisor
791 $a Ph.D.
792 $a 2002
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