PUBLICATION
Conservation of Zebrafish MicroRNA-145 and Its Role during Neural Crest Cell Development
- Authors
- Steeman, T.J., Rubiolo, J.A., Sánchez, L.E., Calcaterra, N.B., Weiner, A.M.J.
- ID
- ZDB-PUB-210703-35
- Date
- 2021
- Source
- Genes 12(7): (Journal)
- Registered Authors
- Calcaterra, Nora
- Keywords
- embryonic development, gene regulatory network, microRNA, neural crest
- MeSH Terms
-
- Animals
- Cell Differentiation
- Craniofacial Abnormalities/etiology
- Craniofacial Abnormalities/metabolism
- Craniofacial Abnormalities/pathology
- Gene Expression Regulation, Developmental*
- Gene Regulatory Networks*
- MicroRNAs/genetics*
- Neural Crest/cytology*
- Neural Crest/metabolism
- Organogenesis*
- Pigmentation Disorders/etiology
- Pigmentation Disorders/metabolism
- Pigmentation Disorders/pathology
- Zebrafish/genetics
- Zebrafish/growth & development*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 34209401 Full text @ Genes (Basel)
Citation
Steeman, T.J., Rubiolo, J.A., Sánchez, L.E., Calcaterra, N.B., Weiner, A.M.J. (2021) Conservation of Zebrafish MicroRNA-145 and Its Role during Neural Crest Cell Development. Genes. 12(7):.
Abstract
The neural crest is a multipotent cell population that develops from the dorsal neural fold of vertebrate embryos in order to migrate extensively and differentiate into a variety of tissues. A number of gene regulatory networks coordinating neural crest cell specification and differentiation have been extensively studied to date. Although several publications suggest a common role for microRNA-145 (miR-145) in molecular reprogramming for cell cycle regulation and/or cellular differentiation, little is known about its role during in vivo cranial neural crest development. By modifying miR-145 levels in zebrafish embryos, abnormal craniofacial development and aberrant pigmentation phenotypes were detected. By whole-mount in situ hybridization, changes in expression patterns of col2a1a and Sry-related HMG box (Sox) transcription factors sox9a and sox9b were observed in overexpressed miR-145 embryos. In agreement, zebrafish sox9b expression was downregulated by miR-145 overexpression. In silico and in vivo analysis of the sox9b 3'UTR revealed a conserved potential miR-145 binding site likely involved in its post-transcriptional regulation. Based on these findings, we speculate that miR-145 participates in the gene regulatory network governing zebrafish chondrocyte differentiation by controlling sox9b expression.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping