ZFIN ID: ZDB-PUB-190701-16
Loss-of-function mutations in the melanocortin-1-receptor (Mc1r) cause disruption of dorso-ventral countershading in teleost fish
Cal, L., Suarez-Bregua, P., Braasch, I., Irion, U., Kelsh, R., Cerdá-Reverter, J.M., Rotllant, J.
Date: 2019
Source: Pigment cell & melanoma research   32(6): 817-828 (Journal)
Registered Authors: Braasch, Ingo, Cerdá-Reverter, José Miguel, Irion, Uwe, Kelsh, Robert, Rotllant, Josep
Keywords: CRISPR, Asip1, Mc1r, chromatophore, countershading, iridophores, melanophores, pigmentation, xanthophores, zebrafish
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Body Patterning/genetics*
  • CRISPR-Cas Systems/genetics
  • Loss of Function Mutation/genetics*
  • Melanophores/metabolism
  • Models, Biological
  • Phenotype
  • Pigmentation/genetics*
  • Receptor, Melanocortin, Type 1/agonists
  • Receptor, Melanocortin, Type 1/chemistry
  • Receptor, Melanocortin, Type 1/genetics*
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish Proteins/metabolism
PubMed: 31251842 Full text @ Pigment Cell Melanoma Res.
The Melanocortin 1 receptor (MC1R) is the central melanocortin receptor involved in vertebrate pigmentation. Mutations in this gene cause variations in coat coloration in amniotes. Additionally, in mammals MC1R is the main receptor for agouti signaling protein (ASIP), making it the critical receptor for the establishment of dorsal-ventral countershading. In fish, Mc1r is also involved in pigmentation but it has been almost exclusively studied in relation to melanosome dispersion activity and as a putative genetic factor involved in dark/light adaptation. However, its role as the crucial component for the Asip1-dependent control of dorsal-ventral pigmentation remains unexplored. Using CRISPR/Cas9 we created mc1r homozygous knockout zebrafish and found that loss-of-function of mc1r causes a reduction of countershading and a general paling of the animals. We find ectopic development of melanophores and xanthophores, accompanied by a decrease in iridophore numbers in the ventral region of mc1r mutants. We also reveal subtle differences in the role of mc1r in repressing pigment cell development between the skin and scale niches in ventral regions This article is protected by copyright. All rights reserved.