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beta-Amyloid precursor protein-b is essential for Mauthner cell development in the zebrafish in a Notch-dependent manner

Journal article
Authors Rakesh Kumar Banote
Malin Edling
F. Eliassen
Petronella Kettunen
Henrik Zetterberg
Alexandra Abramsson
Published in Developmental Biology
Volume 413
Issue 1
Pages 26-38
ISSN 0012-1606
Publication year 2016
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Department of Chemistry and Molecular Biology
Pages 26-38
Language en
Links dx.doi.org/10.1016/j.ydbio.2016.03....
Keywords APP function, Mauthner cell, Development, Zebrafish, Hindbrain, neural stem/progenitor cells, green fluorescent protein, app, intracellular domain, alzheimers-disease, lateral inhibition, gamma-secretase, controls proliferation, embryonic-development, neurogenic phenotype, genomic organization, Developmental Biology
Subject categories Biological Sciences

Abstract

Amyloid precursor protein (APP) is a transmembrane glycoprotein that has been the subject of intense research because of its implication in Alzheimer's disease. However, the physiological function of APP in the development and maintenance of the central nervous system remains largely unknown. We have previously shown that the APP homologue in zebrafish (Danio rerio), Appb, is required for motor neuron patterning and formation. Here we study the function of Appb during neurogenesis in the zebrafish hindbrain. Partial knockdown of Appb using antisense morpholino oligonucleotides blocked the formation of the Mauthner neurons, uni- or bilaterally, with an aberrant behavior as a consequence of this cellular change. The Appb morphants had decreased neurogenesis, increased notch signaling and notch] a expression at the expense of deltaA/D expression. The Mauthner cell development could be restored either by a general decrease in Notch signaling through gamma-secretase inhibition or by a partial knock down of Notch1a. Together, this demonstrates the importance of Appb in neurogenesis and for the first time shows the essential requirement of Appb in the formation of a specific cell type, the Mauthner cell, in the hindbrain during development. Our results suggest that Appb-regulated neurogenesis is mediated through balancing the Notch1a signaling pathway and provide new insights into the development of the Mauthner cell.

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