PUBLICATION

tal1 regulates the formation of intercellular junctions and the maintenance of identity in the endocardium

Authors
Schumacher, J.A., Bloomekatz, J., Garavito-Aguilar, Z.V., and Yelon, D.
ID
ZDB-PUB-131029-15
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
  • Heart Atria/embryology
  • Heart Atria/metabolism
  • Basic Helix-Loop-Helix Transcription Factors/metabolism*
  • Animals
  • Zebrafish Proteins/metabolism*
  • Morphogenesis
  • Proto-Oncogene Proteins/metabolism*
  • Intercellular Junctions/metabolism*
  • Myocardium/metabolism
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Endocardium/embryology*
  • Endocardium/metabolism*
  • Endocardium/pathology
  • Endocardium/transplantation
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental
(all 17)
PubMed
24075907 Full text @ Dev. Biol.
Abstract
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.
Genes / Markers
Figures
Figure Gallery (11 images) / 2
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
s6
    Deficiency
    s896TgTransgenic Insertion
      sd12TgTransgenic Insertion
        sk74TgTransgenic Insertion
          twu277TgTransgenic Insertion
            y7TgTransgenic Insertion
              zn1TgTransgenic Insertion
                1 - 7 of 7
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                Human Disease / Model
                No data available
                Sequence Targeting Reagents
                Target Reagent Reagent Type
                tal1MO5-tal1MRPHLNO
                tal1MO6-tal1MRPHLNO
                1 - 2 of 2
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                Fish
                Antibodies
                Orthology
                No data available
                Engineered Foreign Genes
                Marker Marker Type Name
                DsRedEFGDsRed
                EGFPEFGEGFP
                grcfpEFGgrcfp
                mCherryEFGmCherry
                1 - 4 of 4
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                Mapping
                No data available