PUBLICATION
Zebrafish snai2 mutants fail to phenocopy morphant phenotypes
- Authors
- Bickers, C., Española, S.D., Grainger, S., Pouget, C., Traver, D.
- ID
- ZDB-PUB-180913-28
- Date
- 2018
- Source
- PLoS One 13: e0202747 (Journal)
- Registered Authors
- Grainger, Stephanie, Traver, David
- Keywords
- none
- MeSH Terms
-
- Amino Acid Sequence
- Zebrafish/genetics
- Zebrafish/growth & development
- Zebrafish/metabolism*
- Embryo, Nonmammalian/metabolism
- Morpholinos/metabolism
- Receptors, Notch/metabolism
- Hematopoietic Stem Cells/cytology
- Hematopoietic Stem Cells/metabolism
- Snail Family Transcription Factors/antagonists & inhibitors
- Snail Family Transcription Factors/genetics*
- Snail Family Transcription Factors/metabolism
- Zebrafish Proteins/antagonists & inhibitors
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- Cell Differentiation
- PAX9 Transcription Factor/metabolism
- Signal Transduction
- Phenotype
- Genotype
- Gene Expression Regulation, Developmental
- Mutagenesis, Site-Directed
- Forkhead Transcription Factors/metabolism
- Animals
- PubMed
- 30208064 Full text @ PLoS One
Citation
Bickers, C., Española, S.D., Grainger, S., Pouget, C., Traver, D. (2018) Zebrafish snai2 mutants fail to phenocopy morphant phenotypes. PLoS One. 13:e0202747.
Abstract
Snail2 is a zinc-finger transcription factor best known to repress expression of genes encoding cell adherence proteins to facilitate induction of the epithelial-to-mesenchymal transition. While this role has been best documented in the developmental migration of the neural crest and mesoderm, here we expand on previously reported preliminary findings that morpholino knock-down of snai2 impairs the generation of hematopoietic stem cells (HSCs) during zebrafish development. We demonstrate that snai2 morphants fail to initiate HSC specification and show defects in the somitic niche of migrating HSC precursors. These defects include a reduction in sclerotome markers as well as in the Notch ligands dlc and dld, which are known to be essential components of HSC specification. Accordingly, enforced expression of the Notch1-intracellular domain was capable of rescuing HSC specification in snai2 morphants. To parallel our approach, we obtained two mutant alleles of snai2. In contrast to the morphants, homozygous mutant embryos displayed no defects in HSC specification or in sclerotome development, and mutant fish survive into adulthood. However, when these homozygous mutants were injected with snai2 morpholino, HSCs were improperly specified. In summary, our morpholino data support a role for Snai2 in HSC development, whereas our mutant data suggest that Snai2 is dispensable for this process. Together, these findings further support the need for careful consideration of both morpholino and mutant phenotypes in studies of gene function.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping