{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T15:33:08Z","timestamp":1770910388432,"version":"3.50.1"},"reference-count":30,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2000,10,1]],"date-time":"2000-10-01T00:00:00Z","timestamp":970358400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Semaphorins comprise a large family of phylogenetically conserved secreted and transmembrane glycoproteins, many of which have been implicated in repulsive axon guidance events. The transmembrane semaphorin Sema-1a in Drosophila is expressed on motor axons and is required for the generation of neuromuscular connectivity. Sema-1a can function as an axonal repellent and mediates motor axon defasciculation. Here, by manipulating the levels of Sema-1a and the cell adhesion molecules fasciclin II (Fas II) and connectin (Conn) on motor axons, we provide further evidence that Sema-1a mediates axonal defasciculation events by acting as an axonally localized repellent and that correct motor axon guidance results from a balance between attractive and repulsive guidance cues expressed on motor neurons.<\/jats:p>","DOI":"10.1093\/genetics\/156.2.723","type":"journal-article","created":{"date-parts":[[2021,4,28]],"date-time":"2021-04-28T05:22:44Z","timestamp":1619587364000},"page":"723-731","source":"Crossref","is-referenced-by-count":70,"title":["Semaphorin-1a Acts in Concert With the Cell Adhesion Molecules Fasciclin II and Connectin to Regulate Axon Fasciculation in Drosophila"],"prefix":"10.1093","volume":"156","author":[{"given":"Hung-Hsiang","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alex S","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alex L","family":"Kolodkin","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2000,10,1]]},"reference":[{"key":"2022010421454628000_R1","doi-asserted-by":"crossref","first-page":"401","DOI":"10.1242\/dev.118.2.401","article-title":"Targeted gene expression as a means of altering cell fates and generating dominant phenotypes","volume":"118","author":"Brand","year":"1993","journal-title":"Development"},{"key":"2022010421454628000_R2","doi-asserted-by":"crossref","first-page":"166","DOI":"10.1038\/374166a0","article-title":"Fasciclin III as a synaptic target recognition molecule in Drosophila","volume":"374","author":"Chiba","year":"1995","journal-title":"Nature"},{"key":"2022010421454628000_R3","doi-asserted-by":"crossref","first-page":"2491","DOI":"10.1073\/pnas.96.5.2491","article-title":"Cloning, expression, and genetic mapping of Sema W, a member of the semaphorin family","volume":"96","author":"Encinas","year":"1999","journal-title":"Proc. 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