Document Detail


TBX5 is required for embryonic cardiac cell cycle progression.
MedLine Citation:
PMID:  16728474     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite the critical importance of TBX5 in normal development and disease, relatively little is known about the mechanisms by which TBX5 functions in the embryonic heart. Our present studies demonstrate that TBX5 is necessary to control the length of the embryonic cardiac cell cycle, with depletion of TBX5 leading to cardiac cell cycle arrest in late G(1)- or early S-phase. Blocking cell cycle progression by TBX5 depletion leads to a decrease in cardiac cell number, an alteration in the timing of the cardiac differentiation program, defects in cardiac sarcomere formation, and ultimately, to cardiac programmed cell death. In these studies we have also established that terminally differentiated cardiomyocytes retain the capacity to undergo cell division. We further show that TBX5 is sufficient to determine the length of the embryonic cardiac cell cycle and the timing of the cardiac differentiation program. Thus, these studies establish a role for TBX5 in regulating the progression of the cardiac cell cycle.
Authors:
Sarah C Goetz; Daniel D Brown; Frank L Conlon
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-05-25
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  133     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-06-09     Completed Date:  2007-01-26     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  2575-84     Citation Subset:  IM    
Affiliation:
Carolina Cardiovascular Biology Center, 5109 Neuroscience Research Building, Chapel Hill, NC 27599-7126, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Cell Cycle / physiology
Cell Division
DNA Primers
In Situ Hybridization
Mitosis
Myocardium / cytology*
Reverse Transcriptase Polymerase Chain Reaction
T-Box Domain Proteins / deficiency,  genetics*
Xenopus / genetics*
Xenopus Proteins / deficiency,  genetics*
Grant Support
ID/Acronym/Agency:
R01 HL075256/HL/NHLBI NIH HHS; R01 HL075256-02/HL/NHLBI NIH HHS; R01 HL075256-03/HL/NHLBI NIH HHS; R21 HL083965-01A1/HL/NHLBI NIH HHS; R21HL083965/HL/NHLBI NIH HHS; T32HL69768/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/DNA Primers; 0/T-Box Domain Proteins; 0/T-box transcription factor 5; 0/Xenopus Proteins
Comments/Corrections

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