Phylotypic Expression of the bHLH Genes Neurogenin2, NeuroD, and Mash1 in the Mouse Embryonic Forebrain

In the anamniote model animals, zebrafish and Xenopus laevis, highly comparable early forebrain expression patterns of proneural basic helix-loop-helix (bHLH) genes relevant for neurogenesis (atonal homologs, i.e., neurogenins/NeuroD and achaete-scute homologs, i.e., Asc1/lash) were previously revealed during a particular period of development (zebrafish: 3 days; frog: stage 48). Neurogenins/NeuroD on the one hand and Ascl1/ash1 on the other hand exhibit essentially mutually exclusive spatial patterns, probably reflecting different positional information received within the neural tube, and appear to underlie glutamatergic versus GABAergic neuronal differentiation, respectively. Significant data suggest that similar complementary localizations of these proneural genes and corresponding differentiation pathways also exist in the mouse, the prominent mammalian model. The present article reports on detailed mouse brain bHLH gene expression patterns to fill existing gaps in the identification of ex-pression domains, especially outside the telencephalon. Clearly, there are strong similarities in the complementarity of territories expressing Ascl1/Mash 1 versus neurogenins/NeuroD in the entire mouse forebrain, except for the pretectal alar plate and basal plate of prosomeres 1-3. The analysis substantiates localization of neurogenins/NeuroD in the pallium, eminentia thalami, and dorsal thalamus, and expression of Ascl1/Mash 1 in the striatal and septal subpallium, preoptic region, ventral thalamus, and hypothalamus, which is highly similar to the situation described in Xenopus and zebrafish. Thus, all three vertebrate model species display a "phylotypic stage or period" corresponding to a temporally and spatially defined control of neurogenesis during forebrain development, ultimately resulting in the differentiation of distinct populations of glutamatergic versus GABAergic neurons. J. Comp. Neurol. 518:851-871, 2010. (C) 2009 Wiley-Liss, Inc.