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dc.contributor.authorDantas, Tiago J.
dc.contributor.authorWang, Yifan
dc.contributor.authorLalor, Pierce
dc.contributor.authorDockery, Peter
dc.contributor.authorMorrison, Ciaran G.
dc.date.accessioned2018-09-20T16:05:05Z
dc.date.available2018-09-20T16:05:05Z
dc.date.issued2011-04-11
dc.identifier.citationDantas, Tiago J. Wang, Yifan; Lalor, Pierce; Dockery, Peter; Morrison, Ciaran G. (2011). Defective nucleotide excision repair with normal centrosome structures and functions in the absence of all vertebrate centrins. The Journal of Cell Biology 193 (2), 307-318
dc.identifier.issn0021-9525,1540-8140
dc.identifier.urihttp://hdl.handle.net/10379/11055
dc.description.abstractThe principal microtubule-organizing center in animal cells, the centrosome, contains centrin, a small, conserved calcium-binding protein unique to eukaryotes. Several centrin isoforms exist and have been implicated in various cellular processes including nuclear export and deoxyribonucleic acid (DNA) repair. Although centrins are required for centriole/basal body duplication in lower eukaryotes, centrin functions in vertebrate centrosome duplication are less clear. To define these roles, we used gene targeting in the hyperrecombinogenic chicken DT40 cell line to delete all three centrin genes in individual clones. Unexpectedly, centrin-deficient cells underwent normal cellular division with no detectable cell cycle defects. Light and electron microscopy analyses revealed no significant difference in centrosome composition or ultrastructure. However, centrin deficiency made DT40 cells highly sensitive to ultraviolet (UV) irradiation, with Cetn3 deficiency exacerbating the sensitivity of Cetn4/Cetn2 double mutants. DNA damage checkpoints were intact, but repair of UV-induced DNA damage was delayed in centrin nulls. These data demonstrate a role for vertebrate centrin in nucleotide excision repair.
dc.publisherRockefeller University Press
dc.relation.ispartofThe Journal of Cell Biology
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Ireland
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/3.0/ie/
dc.subjectgroup-c protein
dc.subjectcell-cycle progression
dc.subjectbasal body duplication
dc.subjectmitotic spindle poles
dc.subjectDNA-damage
dc.subjectchlamydomonas-reinhardtii
dc.subjectmicrotubule organization
dc.subjecthomologous recombination
dc.subjectmolecular-cloning
dc.subjectmammalian-cells
dc.titleDefective nucleotide excision repair with normal centrosome structures and functions in the absence of all vertebrate centrins
dc.typeArticle
dc.identifier.doi10.1083/jcb.201012093
dc.local.publishedsourcehttp://jcb.rupress.org/content/193/2/307.full.pdf
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