Mechanisms of illegitimate recombination

Ehrlich, S. Dusko; Bierne, Hélène; d’Alençon, Emmanuelle; Vilette, Didier; Petranović, Mirjana; Naveilhan, Philippe; Michel, Bertrand

doi:10.1016/0378-1119(93)90061-7

Cited by 88 publications

(74 citation statements)

References 30 publications

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“…This, if the RET/PTC intrachromosomal inversion arose as a result of activation of the recombination machinery or errors in cleavage by enzymes that cut and join DNA (such as topoisomerase II), one would expect the breaks to be located within recombinase signal sequences at both participating loci, to have similarity in sequences at the breakpoints, or to be clustered at certain speci®c hypersensitive DNA regions such as AT-rich regions, Alu repeats, repeated purine/pyrimidine tracts, and other chromosomal regions with increased lability (fragile) sites (Ehrlich et al, 1993;Stary and Sarasin, 1992;Hyrien et al, 1987). By contrast, our results indicate that in post-Chernobyl tumors the RET/PTC breakpoints were distributed relatively randomly across the respective introns, except for clustering in the Alu sequences of one of the two contributing genes, with no breakpoints occurring at exactly the same base or within an identical sequence in any of the 12 tumors.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal breakpoint positions suggest a direct role for radiation in inducing illegitimate recombination between the ELE1 and RET genes in radiation-induced thyroid carcinomas

et al. 1999

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The RET/PTC3 rearrangement is formed by fusion of the ELE1 and RET genes, and is highly prevalent in radiation-induced post-Chernobyl papillary thyroid carcinomas. We characterized the breakpoints in the ELE1 and RET genes in 12 post-Chernobyl pediatric papillary carcinomas with known RET/PTC3 rearrangement. We found that the breakpoints within each intron were distributed in a relatively random fashion, except for clustering in the Alu regions of ELE1. None of the breakpoints occurred at the same base or within a similar sequence. There was also no evidence of preferential cleavage in AT-rich regions or other target DNA sites implicated in illegitimate recombination in mammalian cells. Modi®cation of sequences at the cleavage sites was minimal, typically involving a 1 ± 3 nucleotide deletion and/or duplication. Surprisingly, the alignment of ELE1 and RET introns in opposite orientation revealed that in each tumor the position of the break in one gene corresponded to the position of the break in the other gene. This tendency suggests that the two genes may lie next to each other but point in opposite directions in the nucleus. Such a structure would facilitate formation of RET/PTC3 rearrangements because a single radiation track could produce concerted breaks in both genes, leading to inversion due to reciprocal exchange via endjoining.

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Section: Discussionmentioning

confidence: 99%

Chromosomal breakpoint positions suggest a direct role for radiation in inducing illegitimate recombination between the ELE1 and RET genes in radiation-induced thyroid carcinomas

et al. 1999

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“…Illegitimate recombination refers to a collection of different reactions generally occurring at closely spaced DNA sequences that share little or no homology (332)(333)(334)(335). This process is RecA independent and takes place when DNA strands anneal in aberrant configurations following a problem in DNA processing (Fig.…”

Section: Mechanisms Of Homologous and Illegitimate Recombinationmentioning

confidence: 99%

Bacterial Genome Instability

Darmon

Leach

2014

Microbiol Mol Biol Rev

345

289

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SUMMARY Bacterial genomes are remarkably stable from one generation to the next but are plastic on an evolutionary time scale, substantially shaped by horizontal gene transfer, genome rearrangement, and the activities of mobile DNA elements. This implies the existence of a delicate balance between the maintenance of genome stability and the tolerance of genome instability. In this review, we describe the specialized genetic elements and the endogenous processes that contribute to genome instability. We then discuss the consequences of genome instability at the physiological level, where cells have harnessed instability to mediate phase and antigenic variation, and at the evolutionary level, where horizontal gene transfer has played an important role. Indeed, this ability to share DNA sequences has played a major part in the evolution of life on Earth. The evolutionary plasticity of bacterial genomes, coupled with the vast numbers of bacteria on the planet, substantially limits our ability to control disease.

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“…In these models, a deletion and a duplication are not reciprocal outcomes. Slipped misalignment is frequently associated with additional symmetry elements flanking direct repeats that can promote pausing of DNA replication, promote strand slippage and stabilize the misaligned sequences (Glickman & Ripley, 1984 ;Trinh & Sinden, 1991, 1993Ehrlich et al, 1993). The requirement for stabilization may be particularly important for slippage at RPS clusters since the large size of RPS units (2n1-2n3 kb) would suggest a relatively unstable loop.…”

Section: Models For Rps Reorganizationmentioning

confidence: 99%

Microevolutionary changes in Candida albicans identified by the complex Ca3 fingerprinting probe involve insertions and deletions of the full-length repetitive sequence RPS at specific genomic sites

et al. 1999

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The 11 kb complex DNA fingerprinting probe Ca3 is effective both in cluster analyses of Candida albicans isolates and in identifying microevolutionary changes in the size of hypervariable genomic fragments. A 26 kb EcoRI fragment of Ca3, the C fragment, retains the capacity to identify these microevolutionary changes, and when the C fragment is cleaved with SacI, the capacity is retained exclusively by a 1 kb subfragment, C1, which contains a partial RPS repeat element. The microevolutionary changes identified by Ca3, therefore, may involve reorganization of RPS elements dispersed throughout the genome. To test this possibility, hypervariable fragments from several strains of C. albicans were sequenced and compared. The results demonstrate that the microevolutionary changes identified by Ca3 are due to the insertion and deletion of full-length tandem RPS elements at specific genomic sites dispersed throughout the C. albicans genome. The RPS elements at these dispersed sites are bordered by the same upstream and downstream sequences. The frequency of recombination was estimated to be one recombination per 1000 cell divisions by following RPS reorganization in vitro. The results are inconsistent with unequal recombination between homologous or heterologous chromosomes, but consistent with intrachromosomal recombination. Two alternative models of intrachromosomal recombination are proposed : unequal sister-chromatid exchange and slipped misalignment at the replication fork.

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Mechanisms of illegitimate recombination

Cited by 88 publications

References 30 publications

Chromosomal breakpoint positions suggest a direct role for radiation in inducing illegitimate recombination between the ELE1 and RET genes in radiation-induced thyroid carcinomas

Chromosomal breakpoint positions suggest a direct role for radiation in inducing illegitimate recombination between the ELE1 and RET genes in radiation-induced thyroid carcinomas

Bacterial Genome Instability

Microevolutionary changes in Candida albicans identified by the complex Ca3 fingerprinting probe involve insertions and deletions of the full-length repetitive sequence RPS at specific genomic sites

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