ZFIN ID: ZDB-PUB-200625-3
Amyloid precursor protein-b facilitates cell adhesion during early development in zebrafish
Banote, R.K., Chebli, J., Şatır, T.M., Varshney, G.K., Camacho, R., Ledin, J., Burgess, S.M., Abramsson, A., Zetterberg, H.
Date: 2020
Source: Scientific Reports   10: 10127 (Journal)
Registered Authors: Burgess, Shawn, Ledin, Johan, Varshney, Gaurav, Zetterberg, Henrik
Keywords: none
MeSH Terms:
  • Amyloid beta-Protein Precursor
  • Animals
  • Cell Adhesion/genetics*
  • Cell Adhesion/physiology*
  • Cells, Cultured
  • Embryo Culture Techniques
  • Embryo, Nonmammalian*
  • Embryonic Development/genetics*
  • Embryonic Development/physiology*
  • Exons/genetics
  • Gene Expression Regulation, Developmental/genetics*
  • Gene Expression Regulation, Developmental/physiology*
  • Mutation
  • Zebrafish/embryology*
  • Zebrafish/genetics*
PubMed: 32576936 Full text @ Sci. Rep.
Understanding the biological function of amyloid beta (Aβ) precursor protein (APP) beyond its role in Alzheimer's disease is emerging. Yet, its function during embryonic development is poorly understood. The zebrafish APP orthologue, Appb, is strongly expressed during early development but thus far has only been studied via morpholino-mediated knockdown. Zebrafish enables analysis of cellular processes in an ontogenic context, which is limited in many other vertebrates. We characterized zebrafish carrying a homozygous mutation that introduces a premature stop in exon 2 of the appb gene. We report that appb mutants are significantly smaller until 2 dpf and display perturbed enveloping layer (EVL) integrity and cell protrusions at the blastula stage. Moreover, appb mutants surviving beyond 48 hpf exhibited no behavioral defects at 6 dpf and developed into healthy and fertile adults. The expression of the app family member, appa, was also found to be altered in appb mutants. Taken together, we show that appb is involved in the initial development of zebrafish by supporting the integrity of the EVL, likely by mediating cell adhesion properties. The loss of Appb might then be compensated for by other app family members to maintain normal development.