{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T19:56:58Z","timestamp":1792526218168,"version":"4.5.0"},"reference-count":50,"publisher":"Society for Neuroscience","issue":"1","license":[{"start":{"date-parts":[[2002,7,1]],"date-time":"2002-07-01T00:00:00Z","timestamp":1025481600000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2002,1,1]]},"abstract":"<jats:p>Growth-associated protein-43 (GAP-43) is a major growth cone protein whose phosphorylation by PKC in response to extracellular guidance cues can regulate F-actin behavior. Here we show that 100% of homozygote GAP-43 (\u2212\/\u2212) mice failed to form the anterior commissure (AC), hippocampal commissure (HC), and corpus callosum (CC)<jats:italic>in vivo<\/jats:italic>. Instead, although midline fusion was normal, selective fasciculation between commissural axons was inhibited, and TAG-1-labeled axons tangled bilaterally into Probst's bundles. Moreover, their growth cones had significantly smaller lamellas and reduced levels of F-actin<jats:italic>in vitro<\/jats:italic>. Likewise, 100% of GAP-43 (+\/\u2212) mice with one disrupted allele also showed defects in HC and CC, whereas the AC was unaffected. Individual GAP-43 (+\/\u2212) mice could be assigned to two groups based on the amount that PKC phosphorylation of GAP-43 was reduced in neocortical neurons. In mice with \u223c1% phosphorylation, the HC and CC were absent, whereas in mice with \u223c10% phosphorylation, the HC and CC were smaller. Both results suggest that PKC-mediated signaling in commissural axons may be defective. However, although Probst's bundles formed consistently at the location of the glial wedge, both GAP-43 (\u2212\/\u2212) and GAP-43 (+\/+) cortical axons were still repulsed by Slit-2<jats:italic>in vitro<\/jats:italic>, precluding failure of this deflective signal from the glial wedge as the source of the phenotype. Nonetheless, the data show that a functional threshold of GAP-43 is required for commissure formation and suggests that failure to regulate F-actin in commissural growth cones may be related to inhibited PKC phosphorylation of GAP-43.<\/jats:p>","DOI":"10.1523\/jneurosci.22-01-00239.2002","type":"journal-article","created":{"date-parts":[[2018,4,5]],"date-time":"2018-04-05T00:15:54Z","timestamp":1522887354000},"page":"239-247","source":"Crossref","is-referenced-by-count":135,"title":["Growth-Associated Protein-43 Is Required for Commissural Axon Guidance in the Developing Vertebrate Nervous System"],"prefix":"10.1523","volume":"22","author":[{"given":"Yiping","family":"Shen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shyamala","family":"Mani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stacy 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