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First published online 25 May 2006
doi: 10.1242/dev.02420

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TBX5 is required for embryonic cardiac cell cycle progression

¹ Carolina Cardiovascular Biology Center, 5109 Neuroscience Research Building, Chapel Hill, NC 27599-7126, USA.
² Department of Biology, Fordham Hall, UNC-Chapel Hill, Chapel Hill, NC 27599-3280, USA.
³ Department of Genetics, Fordham Hall, UNC-Chapel Hill, Chapel Hill, NC 27599-3280, USA.

^* Author for correspondence (e-mail: frank_conlon{at}med.unc.edu)

Accepted 28 April 2006

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 G₁- 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.

Key words: Tbx5, Holt-Oram Syndrome, Cardiogenesis, Cardiac, Heart, Xenopus, Cell cycle, S-phase, Proliferation, T-box

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