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β-Amyloid precursor protein-b is essential for Mauthner cell development in the zebrafish in a Notch-dependent manner.
Dev Biol. 2016 May 01; 413(1):26-38.DB

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 notch1a expression at the expense of deltaA/D expression. The Mauthner cell development could be restored either by a general decrease in Notch signaling through γ-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.

Authors+Show Affiliations

Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, S-41345 Gothenburg, Sweden. Electronic address: rakesh.k.banote@neuro.gu.se.Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, S-41345 Gothenburg, Sweden.The Faculty of Science, Department of Chemistry and Molecular Biology, University of Gothenburg, 40530 Gothenburg, Sweden.Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, S-41345 Gothenburg, Sweden.Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, S-41345 Gothenburg, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N3BG, United Kingdom.Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, S-41345 Gothenburg, Sweden. Electronic address: alexandra.abramsson@neuro.gu.se.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26994945

Citation

Banote, Rakesh Kumar, et al. "Β-Amyloid Precursor Protein-b Is Essential for Mauthner Cell Development in the Zebrafish in a Notch-dependent Manner." Developmental Biology, vol. 413, no. 1, 2016, pp. 26-38.
Banote RK, Edling M, Eliassen F, et al. Β-Amyloid precursor protein-b is essential for Mauthner cell development in the zebrafish in a Notch-dependent manner. Dev Biol. 2016;413(1):26-38.
Banote, R. K., Edling, M., Eliassen, F., Kettunen, P., Zetterberg, H., & Abramsson, A. (2016). Β-Amyloid precursor protein-b is essential for Mauthner cell development in the zebrafish in a Notch-dependent manner. Developmental Biology, 413(1), 26-38. https://doi.org/10.1016/j.ydbio.2016.03.012
Banote RK, et al. Β-Amyloid Precursor Protein-b Is Essential for Mauthner Cell Development in the Zebrafish in a Notch-dependent Manner. Dev Biol. 2016 May 1;413(1):26-38. PubMed PMID: 26994945.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - β-Amyloid precursor protein-b is essential for Mauthner cell development in the zebrafish in a Notch-dependent manner. AU - Banote,Rakesh Kumar, AU - Edling,Malin, AU - Eliassen,Fredrik, AU - Kettunen,Petronella, AU - Zetterberg,Henrik, AU - Abramsson,Alexandra, Y1 - 2016/03/16/ PY - 2015/11/04/received PY - 2016/03/10/accepted PY - 2016/3/21/entrez PY - 2016/3/21/pubmed PY - 2016/9/9/medline KW - APP function KW - Development KW - Hindbrain KW - Mauthner cell KW - Zebrafish SP - 26 EP - 38 JF - Developmental biology JO - Dev. Biol. VL - 413 IS - 1 N2 - 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 notch1a expression at the expense of deltaA/D expression. The Mauthner cell development could be restored either by a general decrease in Notch signaling through γ-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. SN - 1095-564X UR - https://www.unboundmedicine.com/medline/citation/26994945/β_Amyloid_precursor_protein_b_is_essential_for_Mauthner_cell_development_in_the_zebrafish_in_a_Notch_dependent_manner_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0012-1606(15)30275-X DB - PRIME DP - Unbound Medicine ER -