Transient activation of the Notch-her15.1 axis plays an important role in the maturation of V2b interneurons.


Journal

Development (Cambridge, England)
ISSN: 1477-9129
Titre abrégé: Development
Pays: England
ID NLM: 8701744

Informations de publication

Date de publication:
27 08 2020
Historique:
received: 05 06 2020
accepted: 20 07 2020
entrez: 29 8 2020
pubmed: 29 8 2020
medline: 24 3 2021
Statut: epublish

Résumé

In the vertebrate ventral spinal cord, p2 progenitors give rise to two interneuron subtypes: excitatory V2a interneurons and inhibitory V2b interneurons. In the differentiation of V2a and V2b cells, Notch signaling promotes V2b fate at the expense of V2a fate. Later, V2b cells extend axons along the ipsilateral side of the spinal cord and express the inhibitory transmitter GABA. Notch signaling has been reported to inhibit the axonal outgrowth of mature neurons of the central nervous system; however, it remains unknown how Notch signaling modulates V2b neurite outgrowth and maturation into GABAergic neurons. Here, we have investigated neuron-specific Notch functions regarding V2b axon growth and maturation into zebrafish GABAergic neurons. We found that continuous neuron-specific Notch activation enhanced V2b fate determination but inhibited V2b axonal outgrowth and maturation into GABAergic neurons. These results suggest that Notch signaling activation is required for V2b fate determination, whereas its downregulation at a later stage is essential for V2b maturation. Accordingly, we found that a Notch signaling downstream gene,

Identifiants

pubmed: 32855202
pii: 147/16/dev191312
doi: 10.1242/dev.191312
pii:
doi:

Substances chimiques

Receptors, Notch 0
Zebrafish Proteins 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2020. Published by The Company of Biologists Ltd.

Déclaration de conflit d'intérêts

Competing interestsThe authors declare no competing or financial interests.

Auteurs

Takamasa Mizoguchi (T)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Michi Fukada (M)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Miku Iihama (M)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Xuehui Song (X)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Shun Fukagawa (S)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Shuhei Kuwabara (S)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Shuhei Omaru (S)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan.

Shin-Ichi Higashijima (SI)

National Institutes of Natural Sciences, Exploratory Research Center on Life and Living Systems, National Institute for Basic Biology, Okazaki, Aichi 444-8787, Japan.
Graduate University for Advanced Studies, Okazaki, Aichi 444-8787, Japan.

Motoyuki Itoh (M)

Graduate School of Pharmaceutical Science, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8675, Japan mito@chiba-u.jp.

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