Removal of Pax6 Partially Rescues the Loss of Ventral Structures in Shh Null Mice (original) (raw)

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Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, New York, NY 10016, USA

Address correspondence to Gord Fishell, Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA. Email: fishell@saturn.med.nyu.edu.

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Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, New York, NY 10016, USA

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Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, New York, NY 10016, USA

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Marc Fuccillo, Michael Rutlin, Gord Fishell, Removal of Pax6 Partially Rescues the Loss of Ventral Structures in Shh Null Mice, Cerebral Cortex, Volume 16, Issue suppl_1, July 2006, Pages i96–i102, https://doi.org/10.1093/cercor/bhk023
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Abstract

Pax6 and Gli3 are dorsally expressed genes that are known to antagonize sonic hedgehog (Shh) activity. We have previously shown that dorsoventral patterning defects seen in _Shh_−/− mutants are rescued in Shh_−/−;Gli3_−/− compound mutants. Here we investigate if the loss of Pax6 can also ameliorate defects seen in _Shh_−/− mutants. In support of this notion, we observe that the fusion of the cerebral vesicles seen in _Shh_−/− mutants is partially corrected in E12.5 Shh_−/−;Pax6_−/− compound mutants. Investigation of pan-ventral markers such as Dlx2 also shows that, unlike _Shh_−/−, a broad domain of expression of this gene is observed in Shh_−/−;Pax6_−/− mice. Interestingly, we observe that while the expression of ER81 in the ventral telencephalon is expanded, the expression of Ebf1 is lost. This suggests that the rescued ventral domain observed in Shh_−/−;Pax6_−/− mice is the dorsal lateral ganglionic eminence region. With regard to dorsal telencephalic patterning, we also observe rescue of the pallial–subpallial boundary, as well as a partial rescue of the dorsal midline. Together, our findings are consistent with Pax6 function being required for aspects of _Gli3_-mediated telencephalic patterning.

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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Topic:

• ganglia
• genes
• mice, knockout
• telencephalon
• brain
• mice
• vesicle
• zinc finger protein gli3
• shh gene

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