PUBLICATION
Lamb1a regulates atrial growth by limiting second heart field addition during zebrafish heart development
- Authors
- Derrick, C.J., Pollitt, E.J.G., Sevilla Uruchurtu, A.S., Hussein, F., Grierson, A.J., Noël, E.S.
- ID
- ZDB-PUB-210928-13
- Date
- 2021
- Source
- Development (Cambridge, England) 148(20): (Journal)
- Registered Authors
- Derrick, Chris, Noël, Emily
- Keywords
- Contractility, Extracellular matrix, Heart development, Laminin, Second heart field, Zebrafish
- MeSH Terms
-
- Animals
- Cell Lineage/physiology
- Gene Expression Regulation, Developmental/physiology
- Heart/physiology*
- Heart Atria/metabolism*
- Heart Defects, Congenital/metabolism
- Laminin/metabolism*
- Morphogenesis/physiology
- Myocardium/metabolism
- Organogenesis/physiology
- Zebrafish/metabolism*
- Zebrafish Proteins/metabolism*
- PubMed
- 34568948 Full text @ Development
Citation
Derrick, C.J., Pollitt, E.J.G., Sevilla Uruchurtu, A.S., Hussein, F., Grierson, A.J., Noël, E.S. (2021) Lamb1a regulates atrial growth by limiting second heart field addition during zebrafish heart development. Development (Cambridge, England). 148(20).
Abstract
During early vertebrate heart development the heart transitions from a linear tube to a complex asymmetric structure, a morphogenetic process which occurs simultaneously with growth of the heart. Cardiac growth during early heart morphogenesis is driven by deployment of cells from the Second Heart Field (SHF) into both poles of the heart. Laminin is a core component of the extracellular matrix (ECM), and although mutations in laminin subunits are linked with cardiac abnormalities, no role for laminin has been identified in early vertebrate heart morphogenesis. We identified tissue-specific expression of laminin genes in the developing zebrafish heart, supporting a role for laminins in heart morphogenesis. Analysis of heart development in lamb1a zebrafish mutant embryos reveals mild morphogenetic defects and progressive cardiomegaly, and that Lamb1a functions to limit heart size during cardiac development by restricting SHF addition. lamb1a mutants exhibit hallmarks of altered haemodynamics, and blocking cardiac contractility in lamb1a mutants rescues heart size and atrial SHF addition. Together this suggests that laminin mediates interactions between SHF deployment and cardiac biomechanics during heart development and growth in the developing embryo.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping