The evolution of the amplified adenylate deaminase 2 domains in Chinese hamster cells suggests the sequential operation of different mechanisms of DNA amplification

Toledo, Franck; Smith, Kathleen A.; Buttin, Gérard; Debatisse, Michèlle

doi:10.1016/0165-1110(92)90012-x

Cited by 34 publications

(30 citation statements)

References 22 publications

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“…These observations are also consistent with the fact that many drug-resistant Chinese hamster variants contain amplified DNA (22,(45)(46)(47).…”

Section: Materuils and Methodssupporting

confidence: 76%

“…(i) The amplified DNA localized distally to the single-copy target gene in the same chromosomal arm has been described for many drug-resistant hamster cells selected with various cytotoxic agents (22, 35, 38-40, 45-47, 51 deletion of the chromosome arm containing amplified DNA has been noted (35). (iii) Frequent sister chromatid fusion and formation of dicentric chromosomes have also been observed to occur in many drug-resistant hamster cell lines (17,22,39,46,51). (iv) The B-F-B mechanism predicts a very large inverted duplication of the chromosome arm between the single-copy locus and the amplified DNA cluster and between each amplification unit within the amplified cluster.…”

mentioning

confidence: 99%

“…(iv) The B-F-B mechanism predicts a very large inverted duplication of the chromosome arm between the single-copy locus and the amplified DNA cluster and between each amplification unit within the amplified cluster. By using multiple DNA probes with two-color FISH, these have indeed been found in the methotrexate (MTX)-and deoxycoformycinresistant lines (22,46).…”

mentioning

confidence: 99%

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Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells.

Kuo¹,

Vyas²,

Jiang³

et al. 1994

Mol. Cell. Biol.

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Recent studies of several drug-resistant Chinese hamster cell lines suggested that a breakage-fusion-bridge mechanism is frequently involved in the amplification of drug resistance genes. These observations underscore the importance of chromosome breakage in the initiation of DNA amplification in mammalian cells. However, the mechanism of this breakage is unknown. Here, we propose that the site of chromosome breakage consistent with the initial event of P-glycoprotein (P-gp) gene amplification via the breakage-fusion-bridge cycle in three independently established multidrug-resistant CHO cells was located at 1q31. This site is a major chromosome fragile site that can be induced by methotrexate and aphidicolin treatments. Pretreatments of CHO cells with methotrexate or aphidicolin enhanced the frequencies of resistance to vinca alkaloid and amplification of the P-gp gene. These observations suggest that chromosome fragile sites play a pivotal role in DNA amplification in mammalian cells. Our data are also consistent with the hypothesis that gene amplification can be initiated by stress-induced chromosome breakage that is independent of modes of action of cytotoxic agents. Drug-resistant variants may arise by their growth advantage due to overproduction of cellular target molecules via gene amplification.

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“…These observations are also consistent with the fact that many drug-resistant Chinese hamster variants contain amplified DNA (22,(45)(46)(47).…”

Section: Materuils and Methodssupporting

confidence: 76%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells.

Kuo¹,

Vyas²,

Jiang³

et al. 1994

Mol. Cell. Biol.

View full text Add to dashboard Cite

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“…Expansion of the initial duplication could subsequently lead to multiplication. As a key feature the amplified gene copies would reside on the same chromosome arm that carries the single-copy gene with the gene present in its normal position in the marker chromosome (27)(28)(29)(30). It is interesting that the amplified gene copies even after long-term selection usually remain on the same chromosome where the single-copy gene is localized (29,31), although the complexity of the amplified structures may be condensed by relatively infrequent secondary events (28).…”

Section: Discussionmentioning

confidence: 99%

“…This structure could be resolved through recombination into intra-or extrachromosomal DNA (25). Inspection of early events by chromosomal in situ hybridization, however, has revealed that initial products of drug-resistance gene amplification can be tens of megabases long (27)(28)(29) and therefore too large to fit extrareplication models. The initial event proposed to account for the duplication of large regions, particularly in the amplification of the carbamoyl-phosphate synthetase 2/aspartate carbamoyltransferase/dihydroorotase gene (28) and the adenylate deaminase 2 gene (30), is based on telomeric fusions and bridge-breakage-fusion cycles (28).…”

Section: Discussionmentioning

confidence: 99%

MYCN is retained in single copy at chromosome 2 band p23-24 during amplification in human neuroblastoma cells.

Corvi

Amler

Savelyeva

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Amplification of the 11q13 region in human carcinoma cell lines: A mechanistic view

Roelofs

Schuuring

Wiegant

et al. 1993

Genes Chromosomes & Cancer

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We previously proposed that a local duplication, not the loss of the subsequently amplified marker from its original site, might be the first step in gene amplification in human cells. It is important to investigate this issue in naturally occurring amplification and when copy numbers are relatively low. We have examined the location of single-copy and amplified 11q13 sequences in cell lines from human breast cancers and squamous cell carcinomas using fluorescence in situ hybridization both with a probe specific for the 11q13 amplifying region and with a chromosome 11-specific library. We show that in most cell lines the 11q13 amplicons are physically linked to chromosome 11 or to a chromosome derived from chromosome 11 by various rearrangements near the 11q13 region. In none of the cell lines were interstitial deletions of 11q13 detected. These results indicate that 11q13 amplification in human tumor cells generally does not involve deletion as the initial step. One cell line with chromosomally located amplified 11q13 sequences contained double minutes that harbored the MYC gene but no 11q13 sequences. This suggests that the genetic outcome and the mechanism of gene amplification are probably dependent on specific DNA sequences rather than on the origin of the cells.

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The evolution of the amplified adenylate deaminase 2 domains in Chinese hamster cells suggests the sequential operation of different mechanisms of DNA amplification

Cited by 34 publications

References 22 publications

Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells.

Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells.

MYCN is retained in single copy at chromosome 2 band p23-24 during amplification in human neuroblastoma cells.

Amplification of the 11q13 region in human carcinoma cell lines: A mechanistic view

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