PUBLICATION
Llgl1 mediates timely epicardial emergence and establishment of an apical laminin sheath around the trabeculating cardiac ventricle
- Authors
- Pollitt, E.J.G., Sánchez-Posada, J., Snashall, C.M., Derrick, C.J., Noël, E.S.
- ID
- ZDB-PUB-240629-4
- Date
- 2024
- Source
- Development (Cambridge, England) 151(13): (Journal)
- Registered Authors
- Noël, Emily
- Keywords
- Epicardium, Extracellular matrix, Heart development, Laminin, Polarity, Zebrafish
- MeSH Terms
-
- Animals
- Cell Polarity
- Heart Ventricles*/embryology
- Heart Ventricles*/metabolism
- Laminin*/genetics
- Laminin*/metabolism
- Mutation/genetics
- Myocytes, Cardiac/cytology
- Myocytes, Cardiac/metabolism
- Pericardium*/cytology
- Pericardium*/embryology
- Pericardium*/metabolism
- Zebrafish*/embryology
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 38940292 Full text @ Development
Citation
Pollitt, E.J.G., Sánchez-Posada, J., Snashall, C.M., Derrick, C.J., Noël, E.S. (2024) Llgl1 mediates timely epicardial emergence and establishment of an apical laminin sheath around the trabeculating cardiac ventricle. Development (Cambridge, England). 151(13):.
Abstract
During heart development, the embryonic ventricle becomes enveloped by the epicardium, which adheres to the outer apical surface of the heart. This is concomitant with onset of ventricular trabeculation, where a subset of cardiomyocytes lose apicobasal polarity and delaminate basally from the ventricular wall. Llgl1 regulates the formation of apical cell junctions and apicobasal polarity, and we investigated its role in ventricular wall maturation. We found that llgl1 mutant zebrafish embryos exhibit aberrant apical extrusion of ventricular cardiomyocytes. While investigating apical cardiomyocyte extrusion, we identified a basal-to-apical shift in laminin deposition from the internal to the external ventricular wall. We find that epicardial cells express several laminin subunits as they adhere to the ventricle, and that the epicardium is required for laminin deposition on the ventricular surface. In llgl1 mutants, timely establishment of the epicardial layer is disrupted due to delayed emergence of epicardial cells, resulting in delayed apical deposition of laminin on the ventricular surface. Together, our analyses reveal an unexpected role for Llgl1 in correct timing of epicardial development, supporting integrity of the ventricular myocardial wall.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping