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First published online September 28, 2006
doi: 10.1242/10.1242/dev.02567

Development 133, 4097-4108 (2006)
Published by The Company of Biologists 2006
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Characterization and function of the bHLH-O protein XHes2: insight into the mechanisms controlling retinal cell fate decision

Marion Sölter1,*, Morgane Locker2,*, Sébastien Boy2, Vincent Taelman3, Eric J. Bellefroid3, Muriel Perron2,{dagger} and Tomas Pieler1,{dagger}

1 DFG-Center of Molecular Physiology of the Brain, Department of Developmental Biochemistry, University of Goettingen, Justus-von-Liebig-Weg 11, 37077 Goettingen, Germany.
2 Laboratoire Gènes, Développement et Neurogenèse, UMR CNRS 8080, Bâtiment 445, Université Paris XI, 91405 Orsay, France.
3 Laboratoire d'Embryologie Moléculaire, Université Libre de Bruxelles, Institut de Biologie et de Médecine Moléculaires (IBMM), rue des Profs. Jeener et Brachet 12, 6041 Gosselies, Belgium.

{dagger} Authors for correspondence (e-mail: muriel.perron{at}ibaic.u-psud.fr and tpieler{at}gwdg.de)

Accepted 4 August 2006

Neurons and glial cells differentiate from common multipotent precursors in the vertebrate retina. We have identified a novel member of the hairy/Enhancer of split [E(spl)] gene family in Xenopus, XHes2, as a regulator to bias retinal precursor cells towards a glial fate. XHes2 expression is predominantly restricted to sensory organ territories, including the retina. Using in vivo lipofection in the optic vesicle, we found that XHes2 overexpression dramatically increases gliogenesis at the expense of neurogenesis. This increase in glial cells correlates with a delayed cell cycle withdrawal of some retinal progenitors. In addition, birthdating experiments suggest that XHes2 deviates some early born cell types towards a glial fate that would normally have given rise to neurons. Conversely, a significant inhibition of glial differentiation is observed upon XHes2 loss of function. The gliogenic activity of XHes2 relies on its ability to inhibit neuronal differentiation by at least two distinct mechanisms: it not only negatively regulates XNgnr1 and NeuroD transcription, but it also physically interacts with a subset of proneural bHLH proteins.

Key words: bHLH, Hes2, Gliogenesis, Neurogenesis, Retina, Cell cycle, Xenopus






© The Company of Biologists Ltd 2006