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Article: TSPYL2 is important for G1 checkpoint maintenance upon DNA damage

TitleTSPYL2 is important for G1 checkpoint maintenance upon DNA damage
Authors
Issue Date2011
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2011, v. 6 n. 6 How to Cite?
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. © 2011 Tao et al.
Persistent Identifierhttp://hdl.handle.net/10722/142317
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
PubMed Central ID
ISI Accession Number ID
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.

References

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
DC FieldValueLanguage
dc.contributor.authorTao, KPen_HK
dc.contributor.authorFong, SWen_HK
dc.contributor.authorLu, Zen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, SYen_HK
dc.date.accessioned2011-10-28T02:42:48Z-
dc.date.available2011-10-28T02:42:48Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 6en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142317-
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.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
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 damageen_HK
dc.typeArticleen_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailChan, SY:sychan@hkucc.hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityChan, SY=rp00356en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0021602en_HK
dc.identifier.pmid21738728-
dc.identifier.pmcidPMC3124543-
dc.identifier.scopuseid_2-s2.0-79959598929en_HK
dc.identifier.hkuros196751en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959598929&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue6en_HK
dc.identifier.spagee21602en_US
dc.identifier.epagee21602en_US
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000292092600061-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTao, KP=54584544900en_HK
dc.identifier.scopusauthoridFong, SW=54583476300en_HK
dc.identifier.scopusauthoridLu, Z=54583882500en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridChan, KW=54583253300en_HK
dc.identifier.scopusauthoridChan, SY=7404255082en_HK

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