PUBLICATION

Dicer1 is required for pigment cell and craniofacial development in zebrafish

Authors
Weiner, A.M.J., Scampoli, N.L., Steeman, T.J., Dooley, C.M., Busch-Nentwich, E.M., Kelsh, R.N., Calcaterra, N.B.
ID
ZDB-PUB-190308-12
Date
2019
Source
Biochimica et biophysica acta. Gene regulatory mechanisms   1862(4): 472-485 (Journal)
Registered Authors
Busch-Nentwich, Elisabeth, Calcaterra, Nora, Dooley, Christopher, Kelsh, Robert
Keywords
Neural crest, Zebrafish, miRNAs, sox10
MeSH Terms
  • 3' Untranslated Regions
  • Animals
  • Apoptosis
  • Cartilage/abnormalities*
  • Cartilage/growth & development
  • Embryo, Nonmammalian/abnormalities
  • Embryo, Nonmammalian/anatomy & histology
  • Gene Expression Regulation
  • Head
  • Larva/anatomy & histology
  • Melanocytes/cytology*
  • Melanocytes/metabolism
  • Microphthalmia-Associated Transcription Factor/genetics
  • Microphthalmia-Associated Transcription Factor/metabolism
  • Monophenol Monooxygenase/metabolism
  • Mutation
  • Neural Crest/cytology
  • Ribonuclease III/genetics
  • Ribonuclease III/physiology*
  • SOXE Transcription Factors/genetics
  • SOXE Transcription Factors/metabolism
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/growth & development
  • Zebrafish/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology*
PubMed
30840854 Full text @ BBA Gene Regulatory Mechanisms
Abstract
The multidomain RNase III endoribonuclease DICER is required for the generation of most functional microRNAs (miRNAs). Loss of Dicer affects developmental processes at different levels. Here, we characterized the zebrafish Dicer1 mutant, dicer1sa9205, which has a single point mutation induced by N-ethyl-N-nitrosourea mutagenesis. Heterozygous dicer1sa9205 developed normally, being phenotypically indistinguishable from wild-type siblings. Homozygous dicer1sa9205 mutants display smaller eyes, abnormal craniofacial development and aberrant pigmentation. Reduced numbers of both iridophores and melanocytes were observed in the head and ventral trunk of dicer1sa9205 homozygotes; the effect on melanocytes was stronger and detectable earlier in development. The expression of microphthalmia-associated transcription factor a (mitfa), the master gene for melanocytes differentiation, was enhanced in dicer1-depleted fish. Similarly, the expression of SRY-box containing gene 10 (sox10), required for mitfa activation, was higher in mutants than in wild types. In silico and in vivo analyses of either sox10 or mitfa 3'UTRs revealed conserved potential miRNA binding sites likely involved in the post-transcriptional regulation of both genes. Based on these findings, we propose that dicer1 participates in the gene regulatory network governing zebrafish melanocyte differentiation by controlling the expression of mitfa and sox10.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping