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Background  Insm1 is a zinc-finger transcription factor transiently expressed throughout the developing nervous system in late progenitors and nascent neurons. Insm1 is also highly expressed in medulloblastomas and other neuroendocrine tumors.    Results  We generated mice lacking the  Insm1  gene and used them to elucidate its role in neurogenic proliferation of the embryonic olfactory epithelium. We found that deletion of  Insm1  results in more apical cells and fewer nascent and mature neurons. In the embryonic olfactory epithelium of  Insm1  mutants we detect fewer basal progenitors, which produce neurons, and more apical progenitors, which at this stage produce additional progenitors. Furthermore, in the mutants we detect fewer progenitors expressing NEUROD1, a marker of terminally dividing, neuronogenic (neuron-producing) progenitors (immediate neuronal precursors), and more progenitors expressing ASCL1, a marker of the transit amplifying progenitors that migrate from the apical to the basal edges of the epithelium while dividing to generate the terminal, neuronogenic progenitors. Finally, with timed administration of nucleoside analogs we demonstrate that the  Insm1  mutants contain fewer terminally dividing progenitors at embryonic day 12.5.    Conclusions  Altogether, these results suggest a role for  Insm1  in promoting the transition of progenitors from apical and proliferative to basal, terminal and neuronogenic. This role appears partially conserved with that of its nematode ortholog,  egl-46 . The similar effects of  Insm1  deletion on progenitors of embryonic olfactory epithelium and cortex point to striking parallels in the development of these neuroepithelia, and particularly between the basal progenitors of olfactory epithelium and the subventricular zone progenitors of cortex.

Insm1promotes the transition of olfactory progenitors from apical and proliferative to basal, terminally dividing and neuronogenic