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Development 129, 831-842 (2002)
© 2002 The Company of Biologists Limited

Math3 and NeuroD regulate amacrine cell fate specification in the retina

Tomoyuki Inoue1,2, Masato Hojo1,*, Yasumasa Bessho1, Yasuo Tano2, Jacqueline E. Lee3 and Ryoichiro Kageyama1,{dagger}

1 Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan
2 Department of Ophthalmology, Osaka University Medical School, Suita 565-0871, Japan
3 Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA
* Present address: Department of Neurosurgery, Kurashiki Central Hospital, Okayama 710-8602, Japan

{dagger}Author for correspondence (e-mail: rkageyam{at}virus.kyoto-u.ac.jp)

Accepted 27 November 2001

The basic helix-loop-helix genes Math3 and NeuroD are expressed by differentiating amacrine cells, retinal interneurons. Previous studies have demonstrated that a normal number of amacrine cells is generated in mice lacking either Math3 or NeuroD. We have found that, in Math3-NeuroD double-mutant retina, amacrine cells are completely missing, while ganglion and Müller glial cells are increased in number. In the double-mutant retina, the cells that would normally differentiate into amacrine cells did not die but adopted the ganglion and glial cell fates. Misexpression studies using the developing retinal explant cultures showed that, although Math3 and NeuroD alone only promoted rod genesis, they significantly increased the population of amacrine cells when the homeobox gene Pax6 or Six3 was co-expressed. These results indicate that Math3 and NeuroD are essential, but not sufficient, for amacrine cell genesis, and that co-expression of the basic helix-loop-helix and homeobox genes is required for specification of the correct neuronal subtype.

Key words: Amacrine cell, bHLH, Homeobox, Pax6, Retina, Mouse




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© The Company of Biologists Ltd 2002