Double-strand break repair and recombination-dependent replication of DNA in bacteriophage T4 in the absence of UvsX recombinase: Replicative resolution pathway

Shcherbakov, Victor P.; Plugina, Lidiya; Shcherbakova, Tamara; Kudryashova, Elena; Sizova, Svetlana

doi:10.1016/j.dnarep.2012.01.016

Cited by 3 publications

(2 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The process of break-induced replication (BIR) is a homologous recombination pathway conserved from phage to eukaryotes [56–58] which serves to repair single-ended double-stranded breaks (seDSBs) such as might arise at collapsed or broken replication forks (Figure 2A). BIR has also been implicated in the recombination-dependent alternative lengthening of telomeres (ALT) [59].…”

Section: The Break-induced Replication Fork Is Unstable and Highly Mumentioning

confidence: 99%

Break‐induced replication links microsatellite expansion to complex genome rearrangements

Leffak

2017

BioEssays

View full text Add to dashboard Cite

The instability of microsatellite DNA repeats is responsible for at least forty neurodegenerative diseases. Recently, Mirkin and colleagues presented a novel mechanism for microsatellite expansions based on break-induced replication (BIR) at sites of microsatellite-induced replication stalling and fork collapse. The BIR model aims to explain single-step, large expansions of CAG/CTG trinucleotide repeats in dividing cells. BIR has been characterized extensively in S. cerevisiae as a mechanism to repair broken DNA replication forks (single-ended DSBs) and degraded telomeric DNA. However, the structural footprints of BIR-like DSB repair have been recognized in human genomic instability and tied to the etiology of diverse developmental diseases; thus, the implications of the paper by Kim et al. extend beyond trinucleotide repeat expansion in yeast and microsatellite instability in human neurological disorders. Significantly, insight into BIR-like repair can explain certain pathways of complex genome rearrangements (CGRs) initiated at non-B form microsatellite DNA in human cancers.

show abstract

Section: The Break-induced Replication Fork Is Unstable and Highly Mumentioning

confidence: 99%

Break‐induced replication links microsatellite expansion to complex genome rearrangements

Leffak

2017

BioEssays

View full text Add to dashboard Cite

show abstract

“…The lethality of gene 49 mutants results from their inability to resolve highly branched DNA formed by recombination into linear duplex DNA packageable into a phage capsid. In the absence of UvsX function, recombination runs via a replication resolution pathway that does not lead to formation of the branched DNA (82) .…”

Section: Enzymes Of Mmr Endonuclease Vii: Recognition and Cuttingmentioning

confidence: 99%

Mismatch repair in recombination of bacteriophage T4

Shcherbakov

2012

BioMolecular Concepts

Self Cite

View full text Add to dashboard Cite

The review focuses on the mechanism of mismatch repair in bacteriophage T4. It was fi rst observed in T4 as an extra recombination mechanism, which contributed to the general recombination only when particular rII mutations were used as genetic markers (high-recombination markers), whereas it was inactive toward other rII mutations (lowrecombination markers). This marker-dependent recombination pathway was identifi ed as a repair of mismatches in recombinational heteroduplexes. Comparison of the structure of markers enabled us to make several specifi c conclusions on the nature of the marker discrimination by the mismatch repair system operating during T4 crosses. First, heteroduplexes with one mismatched base pair (either of transition or of transversion type) as well as single-nucleotide mismatches of indel type are not effi ciently repaired. Second, among the repairable mismatches, those with two or more contiguous mismatched nucleotides are the most effectively repaired, whereas insertion of one correct pair between two mismatched ones reduces the repairability. Third, heteroduplexes containing insertion mutations are repaired asymmetrically, the longer strand being preferentially removed. Fourth, the sequence environment is an important factor. Inspection of the sequences fl anking mismatches shows that runs of A:T pairs directly neighboring the mismatches greatly promote repair. The mismatch is recognized by T4 endonuclease VII and nicked on the 3 ′ side. The nonpaired 3 ′ terminus is attacked by the proofreading 3 ′ → 5 ′ exonuclease of T4 DNA polymerase that removes the mismatched nucleotides along with several ( ∼ 25) complementary nucleotides (the repair tract) and then switches to polymerization. The residual nick is ligated by DNA ligase (gp30). Most probably, the T4 system repairs replication and other mismatches as well; however, it might not discriminate old and new DNA strands and so does not seem to be aimed at repair of replication errors, in contrast to the most commonly studied examples of mismatch repair.

show abstract

Double-strand break repair and genetic recombination in topoisomerase and primase mutants of bacteriophage T4

Shcherbakov¹,

Kudryashova²

2014

DNA Repair

View full text Add to dashboard Cite

Double-strand break repair and recombination-dependent replication of DNA in bacteriophage T4 in the absence of UvsX recombinase: Replicative resolution pathway

Cited by 3 publications

References 50 publications

Break‐induced replication links microsatellite expansion to complex genome rearrangements

Break‐induced replication links microsatellite expansion to complex genome rearrangements

Mismatch repair in recombination of bacteriophage T4

Double-strand break repair and genetic recombination in topoisomerase and primase mutants of bacteriophage T4

Contact Info

Product

Resources

About