Tbx20, Smads, and the atrioventricular canal.

摘要

Specification of chamber and nonchamber myocardium in the forming vertebrate heart is a crucial lineage decision on which most of the functional architecture of the mature organ is built. Members of the T-box (Tbx) gene family are decisive players in this early myocardial dichotomy by either promoting (Tbx5, Tbx20) or inhibiting (Tbx2, Tbx3) the chamber gene program in the early heart tube. Because Tbx5 and Tbx20 are widely expressed in the linear heart tube, localized expression of Tbx2 and Tbx3 in regions fated to become primary myocardium of the atrioventricular canal and outflow tract is crucial to localize the chambers. Here, we will review recent findings that suggest an important role for Tbx20 and Bmp2/Smad signaling in restricting Tbx2 activation to the atrioventricular canal and outflow tract. Surprisingly, Tbx20 does not act as a direct transcriptional repressor of Tbx2 but sequesters receptor-activated Smad factors of the Bmp signaling pathway to prevent precocious Tbx2 transcription.