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Sel1l knockdown negatively influences zebrafish embryos endothelium
Author(s) -
Barbieri Andrea,
Carra Silvia,
De Blasio Pasquale,
Cotelli Franco,
Biunno Ida
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26366
Subject(s) - zebrafish , microbiology and biotechnology , danio , morpholino , biology , endoplasmic reticulum , embryonic stem cell , gene knockdown , organogenesis , embryo , endoplasmic reticulum associated protein degradation , enhancer , progenitor cell , stem cell , gene , unfolded protein response , genetics , gene expression
SEL1L (suppressor/enhancer of Lin‐12‐like) is a highly conserved gene associated with the endoplasmic reticulum‐associated degradation (ERAD) pathway and involved in mediating the balance between stem cells self‐renewal and differentiation of neural progenitors. It has been recently shown that SEL1L KO mice are embryonic lethal and display altered organogenesis. To better characterize the function of SEL1L in the early stages of embryonic development, we turned to the zebrafish model ( Danio rerio ). After exploring sel1l expression by RT‐PCR and in situ hybridization, we employed a morpholino‐mediated down‐regulation approach. Results showed extensive impairments in the vasculature, which supports the mice knock‐out findings.