PUBLICATION

The zebrafish cohesin protein Sgo1 is required for cardiac function and eye development

Authors
Kamel, S.M., Broekman, S., Tessadori, F., van Wijk, E., Bakkers, J.
ID
ZDB-PUB-220312-4
Date
2022
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   251(8): 1357-1367 (Journal)
Registered Authors
Bakkers, Jeroen, van Wijk, Erwin
Keywords
Sgo1, cohesinopathy, heart defect, retinal defect, shugoshin, zebrafish
MeSH Terms
  • Animals
  • Cell Cycle Proteins/physiology
  • Centromere*/metabolism
  • Chromatids/metabolism
  • Chromosomal Proteins, Non-Histone/genetics
  • Zebrafish*/genetics
PubMed
35275424 Full text @ Dev. Dyn.
Abstract
Cohesinopathies is a term that refers to/covers rare genetic diseases caused by mutations in the cohesin complex proteins. The cohesin complex is a multi-protein complex that facilitates different aspects of cell division, gene transcription, DNA damage repair and chromosome architecture. Shugoshin proteins prevent the cohesin complex from premature dissociation from chromatids during cell division. Patients with a homozygous missense mutation in SGO1, which encodes for Shugoshin1, have problems with normal pacing of the heart and gut.
To study the role of shugoshin during embryo development, we mutated the zebrafish sgo1 gene. Homozygous sgo1 mutant embryos display various phenotypes related to different organs, including a reduced heart rate accompanied by reduced cardiac function. In addition, sgo1 mutants are vision-impaired as a consequence of structurally defective and partially non-functional photoreceptor cells. Furthermore, the sgo1 mutants display reduced food intake and early lethality.
We have generated a zebrafish model of Sgo1 that showed its importance during organ development and function. This article is protected by copyright. All rights reserved.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping