File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Microtubule breakage is not a major mechanism for resolving end-to-end chromosome fusions generated by telomere dysfunction during the early process of immortalization

TitleMicrotubule breakage is not a major mechanism for resolving end-to-end chromosome fusions generated by telomere dysfunction during the early process of immortalization
Authors
Issue Date2007
PublisherSpringer Verlag. The Journal's web site is located at http://www.springeronline.com/sgw/cda/frontpage/0,10735,5-40109-70-1066702-0,00.html
Citation
Chromosoma, 2007, v. 116 n. 6, p. 557-568 How to Cite?
AbstractTelomeres, the terminal chromosomal structure crucial for maintaining genomic integrity, shorten with deoxyribonucleic acid replications in most human somatic cells. Chromosomes carrying critically short telomeres tend to form end-to-end fusions, which are subject to breakage during cell division. However, it remains obscure how such telomere-mediated fusions are resolved during the process of immortalization, which is an early and indispensable step toward cancer. It has been hypothesized that the breakage could occur at either the microtubule or chromatid, causing numerical or structural chromosome instability, respectively. In this paper, we show that although the distributions of chromosomal segment losses or gains involved in structural aberrations were significantly correlated with the profiles of critically short telomeres in human epithelial cells undergoing immortalization, no such association was detected for whole-chromosome losses or gains in either metaphase or interphase cells. By distinguishing between homologues, we further showed that the specific homologues with critically short telomeres and frequent end-to-end fusions were not preferentially involved in respective whole-chromosome losses or gains. Our data therefore demonstrate that microtubule breakage is not a major mechanism for resolving chromosomal end-to-end fusions in human cells undergoing immortalization. An important implication of this finding is that microtubule-kinetochore attachment is stronger than the chromosome structure. © Springer-Verlag 2007.
Persistent Identifierhttp://hdl.handle.net/10722/67557
ISSN
2015 Impact Factor: 4.303
2015 SCImago Journal Rankings: 3.397
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:56:12Z-
dc.date.available2010-09-06T05:56:12Z-
dc.date.issued2007en_HK
dc.identifier.citationChromosoma, 2007, v. 116 n. 6, p. 557-568en_HK
dc.identifier.issn0009-5915en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67557-
dc.description.abstractTelomeres, the terminal chromosomal structure crucial for maintaining genomic integrity, shorten with deoxyribonucleic acid replications in most human somatic cells. Chromosomes carrying critically short telomeres tend to form end-to-end fusions, which are subject to breakage during cell division. However, it remains obscure how such telomere-mediated fusions are resolved during the process of immortalization, which is an early and indispensable step toward cancer. It has been hypothesized that the breakage could occur at either the microtubule or chromatid, causing numerical or structural chromosome instability, respectively. In this paper, we show that although the distributions of chromosomal segment losses or gains involved in structural aberrations were significantly correlated with the profiles of critically short telomeres in human epithelial cells undergoing immortalization, no such association was detected for whole-chromosome losses or gains in either metaphase or interphase cells. By distinguishing between homologues, we further showed that the specific homologues with critically short telomeres and frequent end-to-end fusions were not preferentially involved in respective whole-chromosome losses or gains. Our data therefore demonstrate that microtubule breakage is not a major mechanism for resolving chromosomal end-to-end fusions in human cells undergoing immortalization. An important implication of this finding is that microtubule-kinetochore attachment is stronger than the chromosome structure. © Springer-Verlag 2007.en_HK
dc.languageengen_HK
dc.publisherSpringer Verlag. The Journal's web site is located at http://www.springeronline.com/sgw/cda/frontpage/0,10735,5-40109-70-1066702-0,00.htmlen_HK
dc.relation.ispartofChromosomaen_HK
dc.subject.meshCell Line, Transformeden_HK
dc.subject.meshCell Transformation, Viral - geneticsen_HK
dc.subject.meshChromosomal Instability - geneticsen_HK
dc.subject.meshChromosome Aberrationsen_HK
dc.subject.meshChromosomes, Human - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMicrotubules - genetics - pathologyen_HK
dc.subject.meshModels, Geneticen_HK
dc.subject.meshTelomere - genetics - pathologyen_HK
dc.titleMicrotubule breakage is not a major mechanism for resolving end-to-end chromosome fusions generated by telomere dysfunction during the early process of immortalizationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-5915&volume=116&spage=557&epage=568&date=2007&atitle=Microtubule+breakage+is+not+a+major+mechanism+for+resolving+end-to-end+chromosome+fusions+generated+by+telomere+dysfunction+during+the+early+process+of+immortalizationen_HK
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM: lmcheung@hku.hken_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00412-007-0120-xen_HK
dc.identifier.pmid17726612-
dc.identifier.scopuseid_2-s2.0-36248963247en_HK
dc.identifier.hkuros138884en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-36248963247&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume116en_HK
dc.identifier.issue6en_HK
dc.identifier.spage557en_HK
dc.identifier.epage568en_HK
dc.identifier.isiWOS:000250880100007-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats