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The Journal of Neuroscience, May 16, 2007, 27(20):5461-5473; doi:10.1523/JNEUROSCI.4046-06.2007

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Development/Plasticity/Repair
Zic1 and Zic3 Regulate Medial Forebrain Development through Expansion of Neuronal Progenitors

Takashi Inoue,¹ Maya Ota,¹ Miyuki Ogawa,¹ Katsuhiko Mikoshiba,² and Jun Aruga¹

¹Laboratory for Comparative Neurogenesis, and ²Laboratory for Developmental Neurobiology, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan

Correspondence should be addressed to Jun Aruga, Laboratory for Comparative Neurogenesis, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan. Email: jaruga{at}brain.riken.jp

The medial telencephalon is a source of neurons that follow distinct tangential trajectories of migration to various structures such as the cerebral cortex, striatum, and olfactory bulb. In the present study, we characterized the forebrain anomalies in Zic1/Zic3 compound mutant mice. Zic1 and Zic3 were strongly expressed in the medial structures, including the septum, medial cerebral cortex, and choroid plexus. Mice homozygous for the Zic1 mutant allele together with the null Zic3 allele showed medial forebrain defects, which were not obvious in either Zic1 or Zic3 single mutants. Absence of both Zic1 and Zic3 caused hypoplasia of the hippocampus, septum, and olfactory bulb. Analysis of the cell cycle revealed that the cell cycle exit rate was increased in the septa of double mutants. Misexpression of Zic3 in the ventricular layer of the cerebral cortex inhibited neuronal differentiation. These results indicated that both Zic1 and Zic3 function in maintaining neural precursor cells in an undifferentiated state. The functions of these genes may be essential to increasing neural cell numbers regionally in the medial telencephalon and to proper mediolateral patterning of the telencephalon.

Key words: forebrain development; neuronal progenitors; neuronal differentiation; olfactory bulb; septum; Zic

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Received Sept. 15, 2006; revised March 23, 2007; accepted April 11, 2007.

Correspondence should be addressed to Jun Aruga, Laboratory for Comparative Neurogenesis, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan. Email: jaruga{at}brain.riken.jp

This article has been cited by other articles:

				D. Maurus and W. A. Harris Zic-associated holoprosencephaly: zebrafish Zic1 controls midline formation and forebrain patterning by regulating Nodal, Hedgehog, and retinoic acid signaling Genes & Dev., June 15, 2009; 23(12): 1461 - 1473. [Abstract] [Full Text] [PDF]

				T. Inoue, M. Ogawa, K. Mikoshiba, and J. Aruga Zic Deficiency in the Cortical Marginal Zone and Meninges Results in Cortical Lamination Defects Resembling Those in Type II Lissencephaly J. Neurosci., April 30, 2008; 28(18): 4712 - 4725. [Abstract] [Full Text] [PDF]

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