Nitrous acid cross-links duplex DNA fragments through deoxyguanosine residues at the sequence 5'-CG

1991 ◽  
Vol 113 (12) ◽  
pp. 4681-4682 ◽  
Author(s):  
James J. Kirchner ◽  
Paul B. Hopkins
1990 ◽  
Vol 112 (6) ◽  
pp. 2459-2460 ◽  
Author(s):  
Julie T. Millard ◽  
Stanley Raucher ◽  
Paul B. Hopkins
Keyword(s):  

2013 ◽  
Vol 41 (13) ◽  
pp. 6774-6781 ◽  
Author(s):  
Atsushi Nishimoto ◽  
Daichi Jitsuzaki ◽  
Kazumitsu Onizuka ◽  
Yosuke Taniguchi ◽  
Fumi Nagatsugi ◽  
...  

1999 ◽  
Vol 121 (21) ◽  
pp. 5081-5082 ◽  
Author(s):  
Eric A. Harwood ◽  
Snorri Th. Sigurdsson ◽  
N. B. Fredrik Edfeldt ◽  
Brian R. Reid ◽  
Paul B. Hopkins

2015 ◽  
Vol 43 (7) ◽  
pp. 3434-3441 ◽  
Author(s):  
Nathan E. Price ◽  
Michael J. Catalano ◽  
Shuo Liu ◽  
Yinsheng Wang ◽  
Kent S. Gates

Biochemistry ◽  
2007 ◽  
Vol 46 (13) ◽  
pp. 3952-3965 ◽  
Author(s):  
Hauh-Jyun Candy Chen ◽  
Chia-Jong Hsieh ◽  
Li-Ching Shen ◽  
Chia-Ming Chang

1998 ◽  
Vol 180 (21) ◽  
pp. 5639-5645 ◽  
Author(s):  
Brigitte Thoms ◽  
Wilfried Wackernagel

ABSTRACT The RecBCD enzyme has a powerful duplex DNA exonuclease activity in vivo. We found that this activity decreased strongly when cells were irradiated with UV light (135 J/m2). The activity decrease was seen by an increase in survival of phage T42 − of about 200-fold (phage T42 − has defective duplex DNA end-protecting gene 2 protein). The activity decrease depended on excision repair proficiency of the cells and a postirradiation incubation. During this time, chromosome fragmentation occurred as demonstrated by pulsed-field gel electrophoresis. In accord with previous observations, it was concluded that the RecBCD enzyme is silenced during interaction with duplex DNA fragments containing Chi nucleotide sequences. The silencing was suppressed by induction or permanent derepression of the SOS system or by the overproduction of single-strand DNA binding protein (from a plasmid with ssb +) which is known to inhibit degradation of chromosomal DNA by cellular DNases. Further, mutations in xonA, recJ, andsbcCD, particularly in the recJ sbcCD andxonA recJ sbcCD combinations, impeded RecBCD silencing. The findings suggest that the DNA fragments had single-stranded tails of a length which prevents loading of RecBCD. It is concluded that in wild-type cells the tails are effectively removed by single-strand-specific DNases including exonuclease I, RecJ DNase, and SbcCD DNase. By this, tailed DNA ends are processed to entry sites for RecBCD. It is proposed that end blunting functions to direct DNA ends into the RecABCD pathway. This pathway specifically activates Chi-containing regions for recombination and recombinational repair.


2016 ◽  
Vol 198 (22) ◽  
pp. 3099-3108 ◽  
Author(s):  
Anthonige Vidya Perera ◽  
James Brian Mendenhall ◽  
Charmain Tan Courcelle ◽  
Justin Courcelle

ABSTRACTDNA interstrand cross-links are complex lesions that covalently link both strands of the duplex DNA. Lesion removal is proposed to be initiated via the UvrABC nucleotide excision repair complex; however, less is known about the subsequent steps of this complex repair pathway. In this study, we characterized the contribution of nucleotide excision repair mutants to survival in the presence of psoralen-induced damage. Unexpectedly, we observed that the nucleotide excision repair mutants exhibit differential sensitivity to psoralen-induced damage, withuvrCmutants being less sensitive than eitheruvrAoruvrB. We show that Cho, an alternative endonuclease, acts with UvrAB and is responsible for the reduced hypersensitivity ofuvrCmutants. We find that Cho's contribution to survival correlates with the presence of DNA interstrand cross-links, rather than monoadducts, and operates at a step after, or independently from, the initial incision during the global repair of psoralen DNA adducts from the genome.IMPORTANCEDNA interstrand cross-links are complex lesions that covalently bind to both strands of the duplex DNA and whose mechanism of repair remains poorly understood. In this study, we show that Cho, an alternative endonuclease, acts with UvrAB and participates in the repair of DNA interstrand cross-links formed in the presence of photoactivated psoralens. Cho's contribution to survival correlates with the presence of DNA interstrand cross-links and operates at a step after, or independently from, the initial incision during the repair process.


2007 ◽  
Vol 129 (7) ◽  
pp. 1852-1853 ◽  
Author(s):  
Sanjay Dutta ◽  
Goutam Chowdhury ◽  
Kent S. Gates

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