PUBLICATION
Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis
- Authors
- Sarmah, S., Hawkins, M.R., Manikandan, P., Farrell, M., Marrs, J.A.
- ID
- ZDB-PUB-221118-3
- Date
- 2022
- Source
- PLoS One 17: e0276255 (Journal)
- Registered Authors
- Marrs, James A.
- Keywords
- none
- MeSH Terms
-
- Animals
- DNA-Binding Proteins/genetics
- Extracellular Matrix*/metabolism
- Gene Expression Regulation, Developmental
- Humans
- Morphogenesis*/genetics
- Proto-Oncogene Proteins c-ets/genetics
- Proto-Oncogene Proteins c-ets/metabolism
- Transcription Factors/metabolism
- Zebrafish*/metabolism
- Zebrafish Proteins*/genetics
- Zebrafish Proteins*/metabolism
- PubMed
- 36383615 Full text @ PLoS One
Citation
Sarmah, S., Hawkins, M.R., Manikandan, P., Farrell, M., Marrs, J.A. (2022) Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis. PLoS One. 17:e0276255.
Abstract
E26 transformation specific (ETS) family transcription factors are expressed during embryogenesis and are involved in various cellular processes such as proliferation, migration, differentiation, angiogenesis, apoptosis, and survival of cellular lineages to ensure appropriate development. Dysregulated expression of many of the ETS family members is detected in different cancers. The human ELF3, a member of the ETS family of transcription factors, plays a role in the induction and progression of human cancers is well studied. However, little is known about the role of ELF3 in early development. Here, the zebrafish elf3 was cloned, and its expression was analyzed during zebrafish development. Zebrafish elf3 is maternally deposited. At different developmental stages, elf3 expression was detected in different tissue, mainly neural tissues, endoderm-derived tissues, cartilage, heart, pronephric duct, blood vessels, and notochord. The expression levels were high at the tissue boundaries. Elf3 loss-of-function consequences were examined by using translation blocking antisense morpholino oligonucleotides, and effects were validated using CRISPR/Cas9 knockdown. Elf3-knockdown produced short and bent larvae with notochord, craniofacial cartilage, and fin defects. The extracellular matrix (ECM) in the fin and notochord was disorganized. Neural defects were also observed. Optic nerve fasciculation (bundling) and arborization in the optic tectum were defective in Elf3-morphants, and fragmentation of spinal motor neurons were evident. Dysregulation of genes encoding ECM proteins and matrix metalloprotease (MMP) and disorganization of ECM may play a role in the observed defects in Elf3 morphants. We conclude that zebrafish Elf3 is required for epidermal, mesenchymal, and neural tissue development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping