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Loss of Gli3 and Shh function disrupts olfactory axon trajectories by Curtis William Balmer; Anthony‐Samuel LaMantia is a Neuroscience article available to read on EtoBox.

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## Abstract The transcriptional regulator __Gli3__ and the secreted signal __Shh__ influence induction, patterning, and differentiation at several sites of mesenchymal/epithelial (M/E) interaction including the limbs, heart, face, and forebrain. We asked whether loss of function of these two genes has specific consequences for early differentiation of the primary olfactory pathway—which comprises both craniofacial and forebrain structures and depends on M/E induction during initial stages of development. Loss of __Gli3__ or __Shh__ function does not compromise several aspects of olfactory receptor neuron (ORN) and olfactory ensheathing cell maturation; however, directed outgrowth of ORN axons and their initial targeting to the telencephalon is altered. In __Gli3__ mutant __extra toes‐Jackson__ (__Xt__^__J__^__Xt__^__J__^) embryos, ORN axons defasciculate and project aberrantly near the forebrain. They rarely enter the central nervous system, and their association with mesenchymal laminin is disrupted. In __Shh__^−/−^embryos, ORN axons exit a single olfactory epithelium (OE) that develops centrally within an altered mesenchymal environment in a dysmorphic proboscis. These axons proj

Who reads Loss of Gli3 and Shh function disrupts olfactory axon trajectories?

Author

Curtis William Balmer; Anthony‐Samuel LaMantia

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square (ISSN 0021-9967)

Published

2004

Language

EN

Field

Neuroscience (Life Sciences)