ZFIN ID: ZDB-PUB-131029-15
tal1 regulates the formation of intercellular junctions and the maintenance of identity in the endocardium
Schumacher, J.A., Bloomekatz, J., Garavito-Aguilar, Z.V., and Yelon, D.
Date: 2013
Source: Developmental Biology   383(2): 214-226 (Journal)
Registered Authors: Bloomekatz, Joshua, Schumacher, Jennifer, Yelon, Deborah
Keywords: Zebrafish, Cardiac morphogenesis, Endocardium, Heart tube assembly, scl
MeSH Terms:
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors/metabolism*
  • Embryo, Nonmammalian/metabolism
  • Endocardium/embryology*
  • Endocardium/metabolism*
  • Endocardium/pathology
  • Endocardium/transplantation
  • Gene Expression Regulation, Developmental
  • Heart Atria/embryology
  • Heart Atria/metabolism
  • Intercellular Junctions/metabolism*
  • Morphogenesis
  • Myocardium/metabolism
  • Proto-Oncogene Proteins/metabolism*
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Zebrafish Proteins/metabolism*
PubMed: 24075907 Full text @ Dev. Biol.
The endocardium forms the inner lining of the heart tube, where it enables blood flow and also interacts with the myocardium during the formation of valves and trabeculae. Although a number of studies have identified regulators in the morphogenesis of the myocardium, relatively little is known about the molecules that control endocardial morphogenesis. Prior work has implicated the bHLH transcription factor Tal1 in endocardial tube formation: in zebrafish embryos lacking Tal1, endocardial cells form a disorganized mass within the ventricle and do not populate the atrium. Through blastomere transplantation, we find that tal1 plays a cell-autonomous role in regulating endocardial extension, suggesting that Tal1 activity influences the behavior of individual endocardial cells. The defects in endocardial behavior in tal1-deficient embryos originate during the earliest steps of endocardial morphogenesis: tal1-deficient endocardial cells fail to generate a cohesive monolayer at the midline and instead pack tightly together into a multi-layered aggregate. Moreover, the tight junction protein ZO-1 is mislocalized in the tal1-deficient endocardium, indicating a defect in intercellular junction formation. In addition, we find that the tal1-deficient endocardium fails to maintain its identity; over time, a progressively increasing number of tal1-deficient endocardial cells initiate myocardial gene expression. However, the onset of defects in intercellular junction formation precedes the onset of ectopic myocardial gene expression in the tal1-deficient endocardium. We therefore propose a model in which Tal1 has distinct roles in regulating the formation of endocardial intercellular junctions and maintaining endocardial identity.