RT Journal Article SR Electronic T1 The Basic Helix-Loop-Helix Gene hesr2 Promotes Gliogenesis in Mouse Retina JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 1265 OP 1273 DO 10.1523/JNEUROSCI.21-04-01265.2001 VO 21 IS 4 A1 Tetsu Satow A1 Soo-Kyung Bae A1 Tomoyuki Inoue A1 Chihiro Inoue A1 Goichi Miyoshi A1 Koichi Tomita A1 Yasumasa Bessho A1 Nobuo Hashimoto A1 Ryoichiro Kageyama YR 2001 UL http://www.jneurosci.org/content/21/4/1265.abstract AB Members of a subclass of hairy/Enhancer of split [E(spl)] homologs, calledhesr genes, are structurally related to another subclass of hairy/E(spl) homologs,Hes genes, which play an important role in neural development. To characterize the roles of hesr genes in neural development, we used the retina as a model system. In situ hybridization analysis indicated that allhesr genes are expressed in the developing retina, but only hesr2 expression is associated spatially with gliogenesis. Each member was then misexpressed with retrovirus in the retinal explant cultures prepared from mouse embryos or neonates, which well mimic in vivo retinal development. Interestingly,hesr2 but not hesr1 orhesr3 promoted gliogenesis while inhibiting rod genesis without affecting cell proliferation or death, suggesting that the cells that normally differentiate into rods adopted the glial fate by misexpression of hesr2. The gliogenic activity ofhesr2 was more profound when it was misexpressed postnatally than prenatally. In addition, double mutation of the neuronal determination genes Mash1 andMath3, which increases Müller glia at the expense of bipolar cells, upregulated hesr2 expression. These results indicate that, among structurally related hesrgenes, only hesr2 promotes glial versus neuronal cell fate specification in the retina and that antagonistic regulation between hesr2 and Mash1–Math3 may determine the ratios of neurons and glia.