PUBLICATION

Loss of Polycomb Repressive Complex 2 Function Alters Digestive Organ Homeostasis and Neuronal Differentiation in Zebrafish

Authors
Raby, L., Völkel, P., Hasanpour, S., Cicero, J., Toillon, R.A., Adriaenssens, E., Van Seuningen, I., Le Bourhis, X., Angrand, P.O.
ID
ZDB-PUB-211129-62
Date
2021
Source
Cells   10(11): (Journal)
Registered Authors
Angrand, Pierre-Olivier, Raby, Ludivine, Völkel, Pamela
Keywords
EED, PRC2, epigenetics, polycomb repression, zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Behavior, Animal
  • Cell Differentiation
  • Digestive System/metabolism*
  • Gene Expression Regulation, Developmental
  • Histones/metabolism
  • Homeostasis*
  • Larva/metabolism
  • Liver/metabolism
  • Lysine/metabolism
  • Methylation
  • Motor Activity
  • Mutation/genetics
  • Neurons/cytology*
  • Neurons/metabolism
  • Organ Specificity
  • Polycomb Repressive Complex 2/deficiency*
  • Polycomb Repressive Complex 2/metabolism
  • Protein Processing, Post-Translational
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Transcription Activator-Like Effector Nucleases/metabolism
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
34831364 Full text @ Cells
Abstract
Polycomb repressive complex 2 (PRC2) mediates histone H3K27me3 methylation and the stable transcriptional repression of a number of gene expression programs involved in the control of cellular identity during development and differentiation. Here, we report on the generation and on the characterization of a zebrafish line harboring a null allele of eed, a gene coding for an essential component of the PRC2. Homozygous eed-deficient mutants present a normal body plan development but display strong defects at the level of the digestive organs, such as reduced size of the pancreas, hepatic steatosis, and a loss of the intestinal structures, to die finally at around 10-12 days post fertilization. In addition, we found that PRC2 loss of function impairs neuronal differentiation in very specific and discrete areas of the brain and increases larval activity in locomotor assays. Our work highlights that zebrafish is a suited model to study human pathologies associated with PRC2 loss of function and H3K27me3 decrease.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping