PUBLICATION
Zebrafish sall1a and sall4 contribute to body elongation
- Authors
- Kawakami, H., Bailey, A., Gavin, E., Gearhart, M.D., Isabella, A.J., Kawakami, Y.
- ID
- ZDB-PUB-250608-9
- Date
- 2025
- Source
- Developmental Biology : (Journal)
- Registered Authors
- Kawakami, Hiroko, Kawakami, Yasuhiko
- Keywords
- body/tail elongation, sall1a, sall4
- Datasets
- GEO:GSE283823
- MeSH Terms
-
- Tail/embryology
- Zebrafish*/embryology
- Zebrafish*/genetics
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- Zebrafish Proteins*/physiology
- Mutation
- Gastrulation
- Transcription Factors*/genetics
- Transcription Factors*/metabolism
- Transcription Factors*/physiology
- Embryo, Nonmammalian/metabolism
- Animals
- Gene Expression Regulation, Developmental
- Mice
- PubMed
- 40482694 Full text @ Dev. Biol.
Citation
Kawakami, H., Bailey, A., Gavin, E., Gearhart, M.D., Isabella, A.J., Kawakami, Y. (2025) Zebrafish sall1a and sall4 contribute to body elongation. Developmental Biology. :.
Abstract
Vertebrate embryos elongate the body after gastrulation. Unlike in mice, which elongate both the trunk and tail after gastrulation, zebrafish embryos complete development of the trunk by the end of gastrulation, followed by tail elongation by proliferation of posteriorly located progenitors. Previous studies have shown that the transcription factors SALL1 and SALL4 redundantly regulate tail elongation in mouse embryos. To test whether sall1a and sall4 also regulate tail elongation in zebrafish, we generated zebrafish mutants for these genes. By 24 hours post-fertilization, sall4 mutant embryos developed normally but exhibited changes in gene expression at the posterior end of the body. sall1a mutants also developed normally by 24 hours post-fertilization. However, embryos mutant for both sall1a and sall4 showed a slight but significant reduction in body length compared to wild-type and sall1a mutant embryos. Our results support a role for sall1a and sall4 in tail elongation in zebrafish, though their contribution appears smaller than that observed in mouse embryos.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping