Homeotic factor ATBF1 induces the cell cycle arrest associated with neuronal differentiation

Jung, Cha-Gyun, Kim, Hye-Jung, Kawaguchi, Makoto, Khanna, Kum Kum, Hida, Hideki, Asai, Kiyofumi, Nishino, Hitoo and Miura, Yutaka (2005) Homeotic factor ATBF1 induces the cell cycle arrest associated with neuronal differentiation. Development, 132 23: 5137-5145. doi:10.1242/dev.02098

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Author Jung, Cha-Gyun
Kim, Hye-Jung
Kawaguchi, Makoto
Khanna, Kum Kum
Hida, Hideki
Asai, Kiyofumi
Nishino, Hitoo
Miura, Yutaka
Title Homeotic factor ATBF1 induces the cell cycle arrest associated with neuronal differentiation
Journal name Development   Check publisher's open access policy
ISSN 0950-1991
Publication date 2005-12
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1242/dev.02098
Open Access Status File (Publisher version)
Volume 132
Issue 23
Start page 5137
End page 5145
Total pages 9
Place of publication Cambridge, U.K.
Publisher Company of Biologists
Language eng
Subject 06 Biological Sciences
0601 Biochemistry and Cell Biology
Abstract The present study aimed to elucidate the function of AT motif-binding factor 1 (ATBF1) during neurogenesis in the developing brain and in primary cultures of neuroepithelial cells and cell lines (Neuro 2A and P19 cells). Here, we show that ATBF1 is expressed in the differentiating field in association with the neuronal differentiation markers beta-tubulin and MAP2 in the day E14.5 embryo rat brain, suggesting that it promotes neuronal differentiation. In support of this, we show that ATBF1 suppresses nestin expression, a neural stem cell marker, and activates the promoter of Neurod1 gene, a marker for neuronal differentiation. Furthermore, we show that in Neuro 2A cells, overexpressed ATBF1 localizes predominantly in the nucleus and causes cell cycle arrest. In P19 cells, which formed embryonic bodies in the floating condition, ATBF1 is mainly cytoplasmic and has no effect on the cell cycle. However, the cell cycle was arrested when ATBF1 became nuclear after transfer of P19 cells onto adhesive surfaces or in isolated single cells. The nuclear localization of ATBF1 was suppressed by treatment with caffeine, an inhibitor of PI(3)K-related kinase activity of ataxa-telangiectasia mutated (ATM) gene product. The cytoplasmic localization of ATBF1 in floating/nonadherent cells is due to CRM1-dependent nuclear export of ATBF1. Moreover, in the embryonic brain ATBF1 was expressed in the cytoplasm of proliferating stem cells on the ventricular zone, where cells are present at high density and interact through cell-to-cell contact. Conversely, in the differentiating field, where cell density is low and extracellular matrix is dense, the cell-to-matrix interaction triggered nuclear localization of ATBF1, resulting in the cell cycle arrest. We propose that ATBF1 plays an important role in the nucleus by organizing the neuronal differentiation associated with the cell cycle arrest.
Keyword Brain
Development
Beta-tubulin
Cells
Caffeine
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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