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First published online 3 March 2004
doi: 10.1242/dev.01071
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Center for Advanced Biotechnology and Medicine and Department of Pediatrics, UMDNJ-Robert Wood Johnson Medical School, 679 Hoes Lane, Piscataway, NJ 08854, USA
* Author for correspondence (e-mail: xiang{at}cabm.rutgers.edu)
Accepted 7 January 2004
The mammalian retina contains numerous morphological and physiological
subtypes of amacrine cells necessary for integrating and modulating visual
signals presented to the output neurons. Among subtypes of amacrine cells
grouped by neurotransmitter phenotypes, the glycinergic and
-aminobutyric acid (GABA)ergic amacrine cells constitute two major
subpopulations. To date, the molecular mechanisms governing the specification
of subtype identity of amacrine cells remain elusive. We report here that
during mouse development, the Barhl2 homeobox gene displays an
expression pattern in the nervous system that is distinct from that of its
homologue Barhl1. In the developing retina, Barhl2
expression is found in postmitotic amacrine, horizontal and ganglion cells,
while Barhl1 expression is absent. Forced expression of Barhl2 in
retinal progenitors promotes the differentiation of glycinergic amacrine
cells, whereas a dominant-negative form of Barhl2 has the opposite effect. By
contrast, they exert no effect on the formation of GABAergic neurons.
Moreover, misexpressed Barhl2 inhibits the formation of bipolar and
Müller glial cells, indicating that Barhl2 is able to function both as a
positive and negative regulator, depending on different types of cells. Taken
together, our data suggest that Barhl2 may function to specify the identity of
glycinergic amacrine cells from competent progenitors during
retinogenesis.
Key words: Barhl2, Homeobox gene, Retina, Retinogenesis, Glycinergic amacrine cell
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