Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE

User menu

  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE
PreviousNext
Articles, Development/Plasticity/Repair

Bre1a, a Histone H2B Ubiquitin Ligase, Regulates the Cell Cycle and Differentiation of Neural Precursor Cells

Yugo Ishino, Yoshitaka Hayashi, Masae Naruse, Koichi Tomita, Makoto Sanbo, Takahiro Fuchigami, Ryoji Fujiki, Kenzo Hirose, Yayoi Toyooka, Toshihiko Fujimori, Kazuhiro Ikenaka and Seiji Hitoshi
Journal of Neuroscience 19 February 2014, 34 (8) 3067-3078; DOI: https://doi.org/10.1523/JNEUROSCI.3832-13.2014
Yugo Ishino
1Division of Neurobiology and Bioinformatics, and
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yoshitaka Hayashi
4Department of Integrative Physiology, Shiga University of Medical Science, Otsu 520-2192, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Masae Naruse
1Division of Neurobiology and Bioinformatics, and
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Koichi Tomita
2Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences, Okazaki 444-8787, Japan,
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Makoto Sanbo
2Center for Genetic Analysis of Behavior, National Institute for Physiological Sciences, Okazaki 444-8787, Japan,
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Takahiro Fuchigami
4Department of Integrative Physiology, Shiga University of Medical Science, Otsu 520-2192, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Ryoji Fujiki
5Institute of Molecular and Cellular Biosciences, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Kenzo Hirose
6Department of Neurobiology, The University of Tokyo, Tokyo 113-0032, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Yayoi Toyooka
7Division of Embryology, National Institute for Basic Biology, Okazaki 444-8787, Japan, and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Toshihiko Fujimori
7Division of Embryology, National Institute for Basic Biology, Okazaki 444-8787, Japan, and
8Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, Kobe 650-0047, Japan
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Kazuhiro Ikenaka
1Division of Neurobiology and Bioinformatics, and
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Seiji Hitoshi
1Division of Neurobiology and Bioinformatics, and
3Department of Physiological Sciences, School of Life Sciences, The Graduate University for Advanced Studies, Okazaki 444-8787, Japan,
4Department of Integrative Physiology, Shiga University of Medical Science, Otsu 520-2192, Japan,
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Abstract

Cell cycle regulation is crucial for the maintenance of stem cell populations in adult mammalian tissues. During development, the cell cycle length in neural stem cells increases, which could be associated with their capabilities for self-renewal. However, the molecular mechanisms that regulate differentiation and cell cycle progression in embryonic neural stem cells remain largely unknown. Here, we investigated the function of Bre1a, a histone H2B ubiquitylation factor, which is expressed in most but not all of neural precursor cells (NPCs) in the developing mouse brain. We found that the knockdown of Bre1a in NPCs lengthened their cell cycle through the upregulation of p57kip2 and the downregulation of Cdk2. In addition, the knockdown of Bre1a increased the expression of Hes5, an effector gene of Notch signaling, through the action of Fezf1 and Fezf2 genes and suppressed the differentiation of NPCs. Our data suggest that Bre1a could be a bifunctional gene that regulates both the differentiation status and cell cycle length of NPCs. We propose a novel model that the Bre1a-negative cells in the ventricular zone of early embryonic brains remain undifferentiated and are selected as self-renewing neural stem cells, which increase their cell cycle time during development.

  • brain development
  • differentiation
  • epigenetics
  • H2B ubiquitylation
  • neural stem cells
  • proliferation
View Full Text
Back to top

In this issue

The Journal of Neuroscience: 34 (8)
Journal of Neuroscience
Vol. 34, Issue 8
19 Feb 2014
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • Advertising (PDF)
  • Ed Board (PDF)
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Bre1a, a Histone H2B Ubiquitin Ligase, Regulates the Cell Cycle and Differentiation of Neural Precursor Cells
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
Bre1a, a Histone H2B Ubiquitin Ligase, Regulates the Cell Cycle and Differentiation of Neural Precursor Cells
Yugo Ishino, Yoshitaka Hayashi, Masae Naruse, Koichi Tomita, Makoto Sanbo, Takahiro Fuchigami, Ryoji Fujiki, Kenzo Hirose, Yayoi Toyooka, Toshihiko Fujimori, Kazuhiro Ikenaka, Seiji Hitoshi
Journal of Neuroscience 19 February 2014, 34 (8) 3067-3078; DOI: 10.1523/JNEUROSCI.3832-13.2014

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
Bre1a, a Histone H2B Ubiquitin Ligase, Regulates the Cell Cycle and Differentiation of Neural Precursor Cells
Yugo Ishino, Yoshitaka Hayashi, Masae Naruse, Koichi Tomita, Makoto Sanbo, Takahiro Fuchigami, Ryoji Fujiki, Kenzo Hirose, Yayoi Toyooka, Toshihiko Fujimori, Kazuhiro Ikenaka, Seiji Hitoshi
Journal of Neuroscience 19 February 2014, 34 (8) 3067-3078; DOI: 10.1523/JNEUROSCI.3832-13.2014
del.icio.us logo Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • Introduction
    • Materials and Methods
    • Results
    • Discussion
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • brain development
  • differentiation
  • epigenetics
  • H2B ubiquitylation
  • neural stem cells
  • proliferation

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

Articles

  • Choice Behavior Guided by Learned, But Not Innate, Taste Aversion Recruits the Orbitofrontal Cortex
  • Maturation of Spontaneous Firing Properties after Hearing Onset in Rat Auditory Nerve Fibers: Spontaneous Rates, Refractoriness, and Interfiber Correlations
  • Insulin Treatment Prevents Neuroinflammation and Neuronal Injury with Restored Neurobehavioral Function in Models of HIV/AIDS Neurodegeneration
Show more Articles

Development/Plasticity/Repair

  • Structural and functional development of inhibitory connections from the medial nucleus of the trapezoid body to the superior paraolivary nucleus
  • Presynaptic kainate receptors onto somatostatin interneurons are recruited by activity throughout development and contribute to cortical sensory adaptation
  • Notch signaling plays a dual role in regulating the neuron-to-oligodendrocyte switch in the developing dorsal forebrain
Show more Development/Plasticity/Repair
  • Home
  • Alerts
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Policy
  • Contact
(JNeurosci logo)
(SfN logo)

Copyright © 2023 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.