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

Autor: Raby L; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Völkel P; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Hasanpour S; Department of Fisheries and Animal Sciences, Faculty of Natural Resources, University of Tehran, Karaj 31587-77871, Iran., Cicero J; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France.; Univ. Artois, UR 2465, Laboratoire de la Barrière Hémato-Encéphalique (LBHE), F-62300 Lens, France., Toillon RA; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Adriaenssens E; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Van Seuningen I; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Le Bourhis X; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France., Angrand PO; Univ. Lille, CNRS, Inserm, CHU Lille, UMR 9020-U 1277 - CANTHER - Cancer Heterogeneity Plasticity and Resistance to Therapies, F-59000 Lille, France.
Jazyk: angličtina
Zdroj: Cells [Cells] 2021 Nov 12; Vol. 10 (11). Date of Electronic Publication: 2021 Nov 12.
DOI: 10.3390/cells10113142
Abstrakt: 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.
Databáze: MEDLINE
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