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Article: TSPYL2 is important for G1 checkpoint maintenance upon DNA damage
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TitleTSPYL2 is important for G1 checkpoint maintenance upon DNA damage
 
AuthorsTao, KP1
Fong, SW1
Lu, Z1
Ching, YP1
Chan, KW1
Chan, SY1
 
Issue Date2011
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2011, v. 6 n. 6 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0021602
 
AbstractNucleosome assembly proteins play important roles in chromatin remodeling, which determines gene expression, cell proliferation and terminal differentiation. Testis specific protein, Y-encoded-like 2 (TSPYL2) is a nucleosome assembly protein expressed in neuronal precursors and mature neurons. Previous studies have shown that TSPYL2 binds cyclin B and inhibits cell proliferation in cultured cells suggesting a role in cell cycle regulation. To investigate the physiological significance of TSPYL2 in the control of cell cycle, we generated mice with targeted disruption of Tspyl2. These mutant mice appear grossly normal, have normal life span and do not exhibit increased tumor incidence. To define the role of TSPYL2 in DNA repair, checkpoint arrest and apoptosis, primary embryonic fibroblasts and thymocytes from Tspyl2 deficient mice were isolated and examined under unperturbed and stressed conditions. We show that mutant fibroblasts are impaired in G1 arrest under the situation of DNA damage induced by gamma irradiation. This is mainly attributed to the defective activation of p21 transcription despite proper p53 protein accumulation, suggesting that TSPYL2 is additionally required for p21 induction. TSPYL2 serves a biological role in maintaining the G1 checkpoint under stress condition. © 2011 Tao et al.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0021602
 
PubMed Central IDPMC3124543
 
ISI Accession Number IDWOS:000292092600061
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, ChinaHKU7323/03M
HKU2/02C
Committee for Research and Conference Grants, The University of Hong Kong
Funding Information:

The work described in this paper was substantially supported by a grant from the Research Grants Council of the Hong Kong Special Administrative Region, China (Project No. HKU7323/03M and HKU2/02C) and partly by the Committee for Research and Conference Grants, The University of Hong Kong. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorTao, KP
 
dc.contributor.authorFong, SW
 
dc.contributor.authorLu, Z
 
dc.contributor.authorChing, YP
 
dc.contributor.authorChan, KW
 
dc.contributor.authorChan, SY
 
dc.date.accessioned2011-10-28T02:42:48Z
 
dc.date.available2011-10-28T02:42:48Z
 
dc.date.issued2011
 
dc.description.abstractNucleosome assembly proteins play important roles in chromatin remodeling, which determines gene expression, cell proliferation and terminal differentiation. Testis specific protein, Y-encoded-like 2 (TSPYL2) is a nucleosome assembly protein expressed in neuronal precursors and mature neurons. Previous studies have shown that TSPYL2 binds cyclin B and inhibits cell proliferation in cultured cells suggesting a role in cell cycle regulation. To investigate the physiological significance of TSPYL2 in the control of cell cycle, we generated mice with targeted disruption of Tspyl2. These mutant mice appear grossly normal, have normal life span and do not exhibit increased tumor incidence. To define the role of TSPYL2 in DNA repair, checkpoint arrest and apoptosis, primary embryonic fibroblasts and thymocytes from Tspyl2 deficient mice were isolated and examined under unperturbed and stressed conditions. We show that mutant fibroblasts are impaired in G1 arrest under the situation of DNA damage induced by gamma irradiation. This is mainly attributed to the defective activation of p21 transcription despite proper p53 protein accumulation, suggesting that TSPYL2 is additionally required for p21 induction. TSPYL2 serves a biological role in maintaining the G1 checkpoint under stress condition. © 2011 Tao et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2011, v. 6 n. 6 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0021602
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0021602
 
dc.identifier.eissn1932-6203
 
dc.identifier.epagee21602
 
dc.identifier.hkuros196751
 
dc.identifier.isiWOS:000292092600061
Funding AgencyGrant Number
Research Grants Council of the Hong Kong Special Administrative Region, ChinaHKU7323/03M
HKU2/02C
Committee for Research and Conference Grants, The University of Hong Kong
Funding Information:

The work described in this paper was substantially supported by a grant from the Research Grants Council of the Hong Kong Special Administrative Region, China (Project No. HKU7323/03M and HKU2/02C) and partly by the Committee for Research and Conference Grants, The University of Hong Kong. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue6
 
dc.identifier.pmcidPMC3124543
 
dc.identifier.pmid21738728
 
dc.identifier.scopuseid_2-s2.0-79959598929
 
dc.identifier.spagee21602
 
dc.identifier.urihttp://hdl.handle.net/10722/142317
 
dc.identifier.volume6
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshApoptosis - genetics - physiology
 
dc.subject.meshCell Cycle Proteins - genetics - metabolism
 
dc.subject.meshDNA Damage - genetics - physiology
 
dc.subject.meshG1 Phase - genetics - physiology
 
dc.subject.meshImmunohistochemistry
 
dc.titleTSPYL2 is important for G1 checkpoint maintenance upon DNA damage
 
dc.typeArticle
 
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<contributor.author>Chan, KW</contributor.author>
<contributor.author>Chan, SY</contributor.author>
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<description.abstract>Nucleosome assembly proteins play important roles in chromatin remodeling, which determines gene expression, cell proliferation and terminal differentiation. Testis specific protein, Y-encoded-like 2 (TSPYL2) is a nucleosome assembly protein expressed in neuronal precursors and mature neurons. Previous studies have shown that TSPYL2 binds cyclin B and inhibits cell proliferation in cultured cells suggesting a role in cell cycle regulation. To investigate the physiological significance of TSPYL2 in the control of cell cycle, we generated mice with targeted disruption of Tspyl2. These mutant mice appear grossly normal, have normal life span and do not exhibit increased tumor incidence. To define the role of TSPYL2 in DNA repair, checkpoint arrest and apoptosis, primary embryonic fibroblasts and thymocytes from Tspyl2 deficient mice were isolated and examined under unperturbed and stressed conditions. We show that mutant fibroblasts are impaired in G1 arrest under the situation of DNA damage induced by gamma irradiation. This is mainly attributed to the defective activation of p21 transcription despite proper p53 protein accumulation, suggesting that TSPYL2 is additionally required for p21 induction. TSPYL2 serves a biological role in maintaining the G1 checkpoint under stress condition. &#169; 2011 Tao et al.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine