ZFIN ID: ZDB-PUB-210123-29
Anterior lateral plate mesoderm gives rise to multiple tissues and requires tbx5a function in left-right asymmetry, migration dynamics, and cell specification of late-addition cardiac cells
Mao, L.M.F., Boyle Anderson, E.A.T., Ho, R.K.
Date: 2021
Source: Developmental Biology   472: 52-66 (Journal)
Registered Authors: Ho, Robert K.
Keywords: Cardiac development, Fate map, Lateral plate mesoderm, Left-right asymmetry, Zebrafish, tbx5a
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Body Patterning/genetics*
  • Branchial Region/metabolism
  • Cell Differentiation/genetics*
  • Cell Movement/genetics*
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Mesoderm/metabolism*
  • Myocytes, Cardiac/metabolism*
  • Organogenesis/genetics
  • Signal Transduction/genetics
  • Transcription Factors/deficiency*
  • Transcription Factors/genetics*
  • Zebrafish/embryology
  • Zebrafish/genetics*
  • Zebrafish/metabolism*
  • Zebrafish Proteins/deficiency*
  • Zebrafish Proteins/genetics*
PubMed: 33482174 Full text @ Dev. Biol.
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ABSTRACT
In this study, we elucidate a single cell resolution fate map in the zebrafish in a sub-section of the anterior Lateral Plate Mesoderm (aLPM) at 18 hpf. Our results show that this tissue is not organized into segregated regions but gives rise to intermingled pericardial sac, peritoneum, pharyngeal arch and cardiac precursors. We further report upon asymmetrical contributions of lateral aLPM-derived heart precursors-specifically that twice as many heart precursors arise from the right side versus the left side of the embryo. Cell tracking analyses and large-scale cell labeling of the lateral aLPM corroborate these differences and show that the observed asymmetries are dependent upon Tbx5a expression. Previously, it was shown that cardiac looping was affected in Tbx5a knock-down and knock-out zebrafish (Garrity et al., 2002; Parrie et al., 2013); our present data also implicate tbx5a function in cell specification, establishment and maintenance of cardiac left-right asymmetry.
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