PUBLICATION
Zebrafish smarcc1a mutants reveal requirements for BAF chromatin remodeling complexes in distinguishing the atrioventricular canal from the cardiac chambers
- Authors
- Auman, H.J., Fernandes, I.H., Berríos-Otero, C.A., Colombo, S., Yelon, D.
- ID
- ZDB-PUB-230422-49
- Date
- 2023
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 253(1): 157-172 (Journal)
- Registered Authors
- Yelon, Deborah
- Keywords
- BAF155, Tbx5, cardiac morphogenesis, cardiac patterning
- MeSH Terms
-
- Animals
- Chromatin Assembly and Disassembly
- Endocardial Cushions*
- Gene Expression Regulation, Developmental
- Heart
- Mammals/metabolism
- Transcription Factors/genetics
- Transcription Factors/metabolism
- Zebrafish*/genetics
- Zebrafish*/metabolism
- Zebrafish Proteins/metabolism
- PubMed
- 37083132 Full text @ Dev. Dyn.
Citation
Auman, H.J., Fernandes, I.H., Berríos-Otero, C.A., Colombo, S., Yelon, D. (2023) Zebrafish smarcc1a mutants reveal requirements for BAF chromatin remodeling complexes in distinguishing the atrioventricular canal from the cardiac chambers. Developmental Dynamics : an official publication of the American Association of Anatomists. 253(1):157-172.
Abstract
Background Essential patterning processes transform the heart tube into a compartmentalized organ with distinct chambers separated by an atrioventricular canal (AVC). This transition involves the refinement of expression of genes that are first found broadly throughout the heart tube and then become restricted to the AVC. Despite the importance of cardiac patterning, we do not fully understand the mechanisms that limit gene expression to the AVC.
Results We show that the zebrafish gene smarcc1a, encoding a BAF chromatin remodeling complex subunit homologous to mammalian BAF155, is critical for cardiac patterning. In smarcc1a mutants, myocardial differentiation and heart tube assembly appear to proceed normally. Subsequently, the smarcc1a mutant heart fails to exhibit refinement of gene expression patterns to the AVC, and the persistence of broad gene expression is accompanied by failure of chamber expansion. In addition to their cardiac defects, smarcc1a mutants lack pectoral fins, indicating similarity to tbx5a mutants. However, comparison of smarcc1a and tbx5a mutants suggests that perturbation of tbx5a function is not sufficient to cause the smarcc1a mutant phenotype.
Conclusions Our data indicate an important role for Smarcc1a-containing chromatin remodeling complexes in regulating the changes in gene expression and morphology that distinguish the AVC from the cardiac chambers. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping