Magnification: gene amplification by an inducible system of sister chromatid exchange

Endow, Sharyn A.; Atwood, K. C.

doi:10.1016/0168-9525(88)90055-8

Cited by 22 publications

(8 citation statements)

References 22 publications

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“…This is the simplest form of amplified repeating units found in mammalian cells and has been found in amplified rRNA genes in Drosophila cells (10) and in amplified dhfr genes in hamster cells (20) (8) are all arranged in tandem arrays. The demonstration of independent amplification events suggests that this area of the genome is under strong selective pressure.…”

Section: Resultsmentioning

confidence: 99%

Amplification of the multidrug resistance gene pfmdr1 in Plasmodium falciparum has arisen as multiple independent events.

Triglia¹,

Foote²,

Kemp³

et al. 1991

Mol. Cell. Biol.

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The multidrug resistance (MDR) phenotype in mammalian tumor cells can involve amplification of mdr genes that results in overexpression of the protein product termed P-glycoprotein. Chloroquine resistance (CQR) in Plasmodium fakciparum has similarities with the MDR phenotype in tumor cells, and some isolates of P. falciparum have amplified levels of the pfmdrl gene. To investigate the nature and origin of pfmdrl amplicons, we have cloned large regions of a 110-kb amplicon from the CQR cloned isolate B8 by using the yeast artificial chromosome system. We have identified and sequenced the breakpoints of the amplicon by a novel method employing inverted polymerase chain reaction that is applicable to analysis of any large-scale repeat. We show that the five copies of the amplicon in this isolate are in a head to tail configuration. A string of 30 A's flank the breakpoints on each side of the amplified segment, suggesting a mechanism for the origin of the tandem amplification. Polymerase chain reaction analysis with oligonucleotides that cross the B8 breakpoint has shown in 26 independent CQR isolates, 16 of which contain amplified copies of pfmdrl, that amplification of the pfmdrl gene in P. falciparum has arisen as multiple independent events. These results suggest that this region of the genome is under strong selective pressure.

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Section: Resultsmentioning

confidence: 99%

Amplification of the multidrug resistance gene pfmdr1 in Plasmodium falciparum has arisen as multiple independent events.

Triglia¹,

Foote²,

Kemp³

et al. 1991

Mol. Cell. Biol.

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“…The incidence of SCE has also been found to be associated with the occurrence of double-minute chromosomes in murine B 16 as well as human tumour cell lines [15]. Unequal sister chromatid recombination is now recognized as a mechanism of gene amplification [9]. Admittedly, most of these observations relate to the B16 tumour variants which have been subjected to selective growth pressures in culture, and there are no data concerning such recombination in tumours grown in vivo.…”

Section: Discussionmentioning

confidence: 99%

Genetic recombination in human melanoma and astrocytoma cell lines involves oncogenes and growth factor genes

Lakshmi

Sherbet

1990

10585 Exp Metast

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We describe here the chromosomal distribution of sister chromatid exchanges (SCEs) in four human tumor cell lines (two melanomas and two astrocytomas), and have mapped the sister chromatid recombination (SCR) sites. A higher incidence of SCR sites than expected on the basis of chromosome length occurred in chromosomes 2, 4, 5 and 15 in both the RPMI 5966 and MEL57 melanoma cell lines, and in chromosomes 1, 5, 13 and 15 of the IJKt and GUVW astrocytoma cell lines. A majority of the recombination sites occurred close to chromosomal fragile sites. A third of these occurred at the same bands as fragile sites. The recombination sites involved the N-ras and the epidermal growth factor gene in the melanomas. In the astrocytomas, the N-ras, Rb and c-mos genes appeared to be involved in the recombination events. The beta 2-microglobulin gene was involved in both astrocytomas and one melanoma. The erbB2 was involved in SCR only in the RPMI melanoma.

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“…The sequence amplification within the Y chromosome may be due to unequal sister chromatid exchange between ayl repeats. Unequal exchanges have also been proposed to explain the amplification of the ribosomal RNA genes in the male germ line of D. melanogaster (Endow and Atwood 1988). However, it cannot be excluded that other mechanisms also are involved.…”

Section: A Model For the Inclusion Of Gypsy Sequences Into The Noosesmentioning

confidence: 99%

Degenerating gypsy retrotransposons in a male fertility gene on the Y chromosome of Drosophila hydei

et al. 1994

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During the evolution of the Y chromosome of Drosophila hydei, retrotransposons became incorporated into the lampbrush loop pairs formed by several of the male fertility genes on this chromosome. Although insertions of retrotransposons are involved in many spontaneous mutations, they do not affect the functions of these genes. We have sequenced gypsy elements that are expressed as constituents of male fertility gene Q in the lampbrush loop pair Nooses. We find that these gypsy elements are all truncated and specifically lost those sequences that may interfere with the continuity of lampbrush loop transcription. Only defective coding regions are found within the loop. Gypsy is not transcribed in loops of many other Drosophila species harboring the family. These results suggest that any contribution of gypsy to the function of male fertility gene Q does not depend on a conserved DNA sequence.

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Magnification: gene amplification by an inducible system of sister chromatid exchange

Cited by 22 publications

References 22 publications

Amplification of the multidrug resistance gene pfmdr1 in Plasmodium falciparum has arisen as multiple independent events.

Amplification of the multidrug resistance gene pfmdr1 in Plasmodium falciparum has arisen as multiple independent events.

Genetic recombination in human melanoma and astrocytoma cell lines involves oncogenes and growth factor genes

Degenerating gypsy retrotransposons in a male fertility gene on the Y chromosome of Drosophila hydei

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