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Article: Sticky anaphase aberrations after G 2-phase arrest of gamma-irradiated human skin fibroblasts: TP53 independence of formation and TP53 dependence of consequences

TitleSticky anaphase aberrations after G 2-phase arrest of gamma-irradiated human skin fibroblasts: TP53 independence of formation and TP53 dependence of consequences
Authors
Issue Date2003
Citation
Radiation Research, 2003, v. 159 n. 1, p. 57-71 How to Cite?
AbstractWe have studied the impact of TP53 status on the extent and nature of chromosome damage seen in human skin fibroblasts after γ irradiation beyond the G 2-phase checkpoint but prior to the G 2-phase checkpoint. Mitotic cells were examined in the absence and presence of treatment with nocodazole and the yield of aberrations was scored as a function of time postirradiation. The results revealed substantially greater damage in the absence of nocodazole, indicating that damage was being masked in its presence. While metaphase aberrations were seen exclusively in the presence of nocodazole, anaphase aberrations were seen principally in its absence. Furthermore, these were mostly of an unseparated, or "sticky", type that showed separation of the chromatids in the centromeric region, indicating normal degradation of cohesin, with retention of adhesion further out on the chromatid arms. Using postirradiation BrdU labeling and the absence of nocodazole, we were able to identify mitotic figures up to the third postirradiation mitosis. Analysis of the data revealed that in cells wildtype for TP53 the aberrant anaphases were lost after the first postirradiation mitosis, although they were still found in gradually decreasing amounts into the second and third postirradiation mitoses in E6-expressing cells. The data indicate that the formation of these sticky anaphases is independent of TP53 status, an observation that is consistent with the TP53 independence of transient G 2-phase arrest. However, the consequences of the formation of these lesions appear to be very different. In the case of cells wild-type for TP53 this is chronic G 1-phase arrest, while in E6 cells it is anaphase catastrophe. © 2003 by Radiation Research Society.
Persistent Identifierhttp://hdl.handle.net/10722/172817
ISSN
2015 Impact Factor: 3.022
2015 SCImago Journal Rankings: 1.493
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRedpath, JLen_US
dc.contributor.authorBengtsson, Uen_US
dc.contributor.authorDesimone, Jen_US
dc.contributor.authorLao, Xen_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorStanbridge, EJen_US
dc.date.accessioned2012-10-30T06:25:05Z-
dc.date.available2012-10-30T06:25:05Z-
dc.date.issued2003en_US
dc.identifier.citationRadiation Research, 2003, v. 159 n. 1, p. 57-71en_US
dc.identifier.issn0033-7587en_US
dc.identifier.urihttp://hdl.handle.net/10722/172817-
dc.description.abstractWe have studied the impact of TP53 status on the extent and nature of chromosome damage seen in human skin fibroblasts after γ irradiation beyond the G 2-phase checkpoint but prior to the G 2-phase checkpoint. Mitotic cells were examined in the absence and presence of treatment with nocodazole and the yield of aberrations was scored as a function of time postirradiation. The results revealed substantially greater damage in the absence of nocodazole, indicating that damage was being masked in its presence. While metaphase aberrations were seen exclusively in the presence of nocodazole, anaphase aberrations were seen principally in its absence. Furthermore, these were mostly of an unseparated, or "sticky", type that showed separation of the chromatids in the centromeric region, indicating normal degradation of cohesin, with retention of adhesion further out on the chromatid arms. Using postirradiation BrdU labeling and the absence of nocodazole, we were able to identify mitotic figures up to the third postirradiation mitosis. Analysis of the data revealed that in cells wildtype for TP53 the aberrant anaphases were lost after the first postirradiation mitosis, although they were still found in gradually decreasing amounts into the second and third postirradiation mitoses in E6-expressing cells. The data indicate that the formation of these sticky anaphases is independent of TP53 status, an observation that is consistent with the TP53 independence of transient G 2-phase arrest. However, the consequences of the formation of these lesions appear to be very different. In the case of cells wild-type for TP53 this is chronic G 1-phase arrest, while in E6 cells it is anaphase catastrophe. © 2003 by Radiation Research Society.en_US
dc.languageengen_US
dc.relation.ispartofRadiation Researchen_US
dc.subject.meshAnaphase - Radiation Effectsen_US
dc.subject.meshCell Cycle - Physiologyen_US
dc.subject.meshCell Lineen_US
dc.subject.meshChromosome Aberrationsen_US
dc.subject.meshChromosomes, Human, Pair 4 - Genetics - Radiation Effectsen_US
dc.subject.meshDna - Genetics - Radiation Effectsen_US
dc.subject.meshFibroblasts - Radiation Effectsen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshG2 Phase - Radiation Effectsen_US
dc.subject.meshGamma Raysen_US
dc.subject.meshGenes, P53en_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridization, Fluorescenceen_US
dc.subject.meshMicronucleus Testsen_US
dc.subject.meshSkin - Radiation Effectsen_US
dc.subject.meshTumor Suppressor Protein P53 - Geneticsen_US
dc.titleSticky anaphase aberrations after G 2-phase arrest of gamma-irradiated human skin fibroblasts: TP53 independence of formation and TP53 dependence of consequencesen_US
dc.typeArticleen_US
dc.identifier.emailWang, X: xqwang@hkucc.hku.hken_US
dc.identifier.authorityWang, X=rp00507en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1667/0033-7587(2003)159[0057:SAAAGP]2.0.CO;2en_US
dc.identifier.pmid12492369-
dc.identifier.scopuseid_2-s2.0-0037229884en_US
dc.identifier.hkuros94326-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037229884&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume159en_US
dc.identifier.issue1en_US
dc.identifier.spage57en_US
dc.identifier.epage71en_US
dc.identifier.isiWOS:000180260800007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRedpath, JL=7006011559en_US
dc.identifier.scopusauthoridBengtsson, U=7005608839en_US
dc.identifier.scopusauthoridDeSimone, J=8785956200en_US
dc.identifier.scopusauthoridLao, X=55161053100en_US
dc.identifier.scopusauthoridWang, X=17343159900en_US
dc.identifier.scopusauthoridStanbridge, EJ=7103249410en_US

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