Show simple item record

dc.contributor.authorKrzywicka-Racka, Anna
dc.contributor.authorSluder, Greenfield
dc.date2022-08-11T08:10:53.000
dc.date.accessioned2022-08-23T17:23:42Z
dc.date.available2022-08-23T17:23:42Z
dc.date.issued2011-07-25
dc.date.submitted2012-04-24
dc.identifier.citationJ Cell Biol. 2011 Jul 25;194(2):199-207. <a href="http://dx.doi.org/10.1083/jcb.201101073">Link to article on publisher's site</a>
dc.identifier.issn0021-9525 (Linking)
dc.identifier.doi10.1083/jcb.201101073
dc.identifier.pmid21788368
dc.identifier.urihttp://hdl.handle.net/20.500.14038/49023
dc.description.abstractWe tested whether cleavage failure as a transient event establishes an incidence of centrosome amplification in cell populations. Five rounds of approximately 30% cytochalasin-induced cleavage failure in untransformed human cell cultures did not establish centrosome amplification in the short or long terms. The progeny of binucleate cells progressively dropped out of the cell cycle and expressed p53/p21, and none divided a fourth time. We also tested whether cleavage failure established centrosome amplification in transformed cell populations. Tetraploid HCT116 p53(-/-) cells eventually all failed cleavage repeatedly and ceased proliferating. HeLa cells all died or arrested within four cell cycles. Chinese hamster ovary cells proliferated after cleavage failure, but five rounds of induced cleavage failure produced a modest increase in the incidence of centrosome amplification in the short term, which did not rise with more cycles of cleavage failure. This incidence dropped to close to control values in the long term despite a 2-6% rate of spontaneous cleavage failure in the progeny of tetraploid cells.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=21788368&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>© 2011 Krzywicka-Racka and Sluder. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).</p>
dc.subjectAnimals
dc.subjectCHO Cells
dc.subjectCell Proliferation
dc.subjectCells, Cultured
dc.subjectCentrosome
dc.subjectCricetinae
dc.subjectCricetulus
dc.subjectHeLa Cells
dc.subjectHumans
dc.subjectImmunohistochemistry
dc.subjectTumor Suppressor Protein p53
dc.subjectCell Biology
dc.titleRepeated cleavage failure does not establish centrosome amplification in untransformed human cells
dc.typeJournal Article
dc.source.journaltitleThe Journal of cell biology
dc.source.volume194
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1009&amp;context=sluder&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/sluder/10
dc.identifier.contextkey2793367
refterms.dateFOA2022-08-23T17:23:43Z
html.description.abstract<p>We tested whether cleavage failure as a transient event establishes an incidence of centrosome amplification in cell populations. Five rounds of approximately 30% cytochalasin-induced cleavage failure in untransformed human cell cultures did not establish centrosome amplification in the short or long terms. The progeny of binucleate cells progressively dropped out of the cell cycle and expressed p53/p21, and none divided a fourth time. We also tested whether cleavage failure established centrosome amplification in transformed cell populations. Tetraploid HCT116 p53(-/-) cells eventually all failed cleavage repeatedly and ceased proliferating. HeLa cells all died or arrested within four cell cycles. Chinese hamster ovary cells proliferated after cleavage failure, but five rounds of induced cleavage failure produced a modest increase in the incidence of centrosome amplification in the short term, which did not rise with more cycles of cleavage failure. This incidence dropped to close to control values in the long term despite a 2-6% rate of spontaneous cleavage failure in the progeny of tetraploid cells.</p>
dc.identifier.submissionpathsluder/10
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages199-207


Files in this item

Thumbnail
Name:
JCB_201101073_1_.pdf
Size:
2.230Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record