Journal
SCIENCE
Volume 320, Issue 5878, Pages 946-949Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1155244
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Funding
- Medical Research Council [G0501173, G9708005] Funding Source: researchfish
- MRC [G0501173, G9708005] Funding Source: UKRI
- Medical Research Council [G9708005, G0800575, G0501173] Funding Source: Medline
- NIMH NIH HHS [R01 MH086147, R01 MH086147-05] Funding Source: Medline
- NINDS NIH HHS [R37 NS031558-15, R37 NS031558] Funding Source: Medline
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Development of axonal tracts requires interactions between growth cones and the environment. Tracts such as the anterior commissure and internal capsule are defective in mice with null mutation of Celsr3. We generated a conditional Celsr3 allele, allowing regional inactivation. Inactivation in telencephalon, ventral forebrain, or cortex demonstrated essential roles for Celsr3 in neurons that project axons to the anterior commissure and subcerebral targets, as well as in cells that guide axons through the internal capsule. When Celsr3 was inactivated in cortex, subcerebral projections failed to grow, yet corticothalamic axons developed normally, indicating that besides guidepost cells, additional Celsr3-independent cues can assist their progression. These observations provide in vivo evidence that Celsr3-mediated interactions between axons and guidepost cells govern axonal tract formation in mammals.
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