Restriction endonucleases do not induce sister-chromatid exchanges in Chinese hamster ovary cells

Morgan, William F.; Chung, Hai Won; Phillips, John W.; Winegar, Richard A.

doi:10.1016/0165-7992(89)90021-3

Cited by 18 publications

(2 citation statements)

References 17 publications

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“…Our results clearly show that, following treatment with with previous reports of SCE induction by RE (Natarajan et al 1985, Obe et al 1994, Folle et al 1992, Balajee & Natarajan 1993) and therefore contrast with the results obtained by Morgan et al (1989). Since the electroporation method causes cell cycle delay (Morgan et al 1990), in our experimental protocol the cells fixed 22 h after electroporation were treated with RE during late G1/early S-phase, as shown by the chromosome-type aberrations observed (Table I), and support the indications of Natarajan et al (1985) and Obe et al (1994), who proposed that this phase of the cell cycle is more prone to induction of SCE by RE than mid or late S-phase.…”

Section: Discussioncontrasting

confidence: 84%

“…Since the electroporation method causes cell cycle delay (Morgan et al 1990), in our experimental protocol the cells fixed 22 h after electroporation were treated with RE during late G1/early S-phase, as shown by the chromosome-type aberrations observed (Table I), and support the indications of Natarajan et al (1985) and Obe et al (1994), who proposed that this phase of the cell cycle is more prone to induction of SCE by RE than mid or late S-phase. In our opinion, this time could be the cause of the disagreement with Morgan et al (1989), since they treated the cells with a series of REs during mid and late S-phase, using the electroporation method and fixation times until 13 h after RE treatment and did not find any increase in the SCE frequencies and only chromatid-type aberrations.…”

Section: Discussionmentioning

confidence: 82%

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On the importance of DNA strand breaks as the first event to initiate sister chromatid exchange (SCE): Experiments with restriction endonucleaseBglI

Ortiz¹,

Piñero²,

Cortés³

1996

Chromosome Res

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The exact molecular mechanism of sister chromatid exchange (SCE) is still unknown, despite the many reports dealing with this cytogenetic end point published in the last 40 years. One point to be investigated is the nature of the original lesion(s) in DNA leading to the production of SCE. Whereas, for chromosomal aberrations, the importance of DNA double-strand breaks has been well established, there is still controversy about the relative importance of strand breaks and base modifications for triggering the process of SCE formation. In the present paper, we have taken advantage of the ability of the restriction endonuclease BglI to induce SCE and have exploited the fact that preincubation with 2,3-butanedione results in the loss of BgiI ability to cut DNA, while it is still able to recognize its sequence in DNA and bind to it, to see whether this alone is enough to initiate SCE formation, or if a physical DNA double-strand break is required. Our results seem to support the necessity of DNA breaks for SCE production.

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Section: Discussioncontrasting

confidence: 84%

Section: Discussionmentioning

confidence: 82%

On the importance of DNA strand breaks as the first event to initiate sister chromatid exchange (SCE): Experiments with restriction endonucleaseBglI

Ortiz¹,

Piñero²,

Cortés³

1996

Chromosome Res

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Specificity of arsenite in potentiating cytogenetic damage induced by the DNA crosslinking agent diepoxybutane

Wiencke

Yager

1992

Environ and Mol Mutagen

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In the present study, the induction of sister chromatid exchanges (SCEs) and chromosomal aberrations were measured in normal human lymphocytes treated with low concentrations of arsenite alone (0.5-2.0 microM) and arsenite in combination with the potent DNA crosslinking agent diepoxybutane (DEB). Experiments were carried out with lymphocytes from blood donors with different sensitivities to SCE induction by DEB. Arsenite, beginning at concentrations as low as 1 microM, increased SCE frequencies; chromosomal aberration frequencies were increased at 2 microM of arsenite. DEB treatments alone increased SCE frequencies and chromosomal aberrations. The yields of chromatid deletions and exchanges in lymphocytes exposed to both arsenite and DEB were markedly increased above the levels expected if the effects of the two agents had been simply additive. The frequencies of chromatid deletions were 4- to 8-fold greater than expected and chromatid exchanges were increased 7- to 40-fold. Chromatid exchanges detected in cells treated with arsenite and DEB were predominately incomplete exchanges. The most dramatic increases in chromatid aberrations were observed in lymphocytes from an individual sensitive to SCE induction by DEB, indicating that individuals may vary in their sensitivity to the co-clastogenic effects of arsenite. At concentrations that dramatically affect aberrations, arsenite had no effect on the induction of SCEs by DEB. These studies suggest a specific interaction of arsenite with the induction or repair of DNA damage produced by DEB that leads to chromosomal aberrations but not to SCEs. Based on the selective chemical reactivity of low concentrations of arsenite with proteins containing vicinal dithiols and the occurrence of these groups within DNA repair proteins, it is proposed that the specific co-clastogenic effects of arsenite may be mediated by its interference with DNA repair activities.

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The Use of Restriction Endonucleases to Study the Mechanisms of Chromosome Damage

Morgan¹,

Winegar

1990

Chromosomal Aberrations

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Restriction endonucleases do not induce sister-chromatid exchanges in Chinese hamster ovary cells

Cited by 18 publications

References 17 publications

On the importance of DNA strand breaks as the first event to initiate sister chromatid exchange (SCE): Experiments with restriction endonucleaseBglI

On the importance of DNA strand breaks as the first event to initiate sister chromatid exchange (SCE): Experiments with restriction endonucleaseBglI

Specificity of arsenite in potentiating cytogenetic damage induced by the DNA crosslinking agent diepoxybutane

The Use of Restriction Endonucleases to Study the Mechanisms of Chromosome Damage

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