ZFIN ID: ZDB-PUB-180523-6
The N-terminal domain of gastrulation brain homeobox 2 (Gbx2) is required for iridophore specification in zebrafish
Hozumi, S., Shirai, M., Wang, J., Aoki, S., Kikuchi, Y.
Date: 2018
Source: Biochemical and Biophysical Research Communications   502(1): 104-109 (Journal)
Registered Authors: Kikuchi, Yutaka
Keywords: Gastrulation homeobox 2 (Gbx2), Iridophore, Melanophore, Neural crest cells, Zebrafish
MeSH Terms:
  • Animals
  • Apoptosis
  • Chromatophores/cytology*
  • Chromatophores/metabolism
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Homeodomain Proteins/chemistry
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism*
  • Neural Crest/cytology*
  • Neural Crest/metabolism
  • Protein Domains
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins/chemistry
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 29787751 Full text @ Biochem. Biophys. Res. Commun.
Although body color pattern formation by pigment cells plays critical roles in animals, pigment cell specification has not yet been fully elucidated. In zebrafish, there are three chromatophores: melanophore, iridophore, and xanthophore, that are derived from neural crest cells (NCCs). A recent study has reported the differentially expressed genes between melanophores and iridophores. Based on transcriptome data, we identified that Gbx2 is required for iridophore specification during development. In support of this, iridophore formation is suppressed by gbx2 knockdown by morpholino antisense oligonucleotide, at 72 h post fertilization (hpf) in zebrafish. Moreover, gbx2 is expressed in sox10-expressing NCCs and guanine crystal plates-containing iridophores during development at 24 and 48 hpf, respectively. In gbx2 knockdown zebrafish embryos, apoptosis of sox10-expressing NCCs was detected at 24 hpf without any effect on the formation of melanophores and xanthophores at 48 hpf. We further observed that the N-terminal domain of Gbx2 is able to rescue the iridophore formation defect caused by gbx2 knockdown. Our study provides insights into the requirement of N-terminal domain of Gbx2 for iridophore specification in zebrafish.