{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T20:08:22Z","timestamp":1791144502545,"version":"4.1.0"},"reference-count":64,"publisher":"The Company of Biologists","issue":"4","license":[{"start":{"date-parts":[[1990,8,1]],"date-time":"1990-08-01T00:00:00Z","timestamp":649468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/www.biologists.com\/user-licence-1-1\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1990,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Expression of the neuronal cell surface glycoprotein Thy-1 has been studied during the development of the olfactory bulb in mice and rats, using in situ hybridisation and immunohistochemistry to follow the appearance of Thy-1 mRNA and protein, respectively. The mRNA was first detected 4 days before birth on all mitral cells, the main projection neuron of the bulb, as they formed a distinct layer and grew dendrites. At no stage was any spatial gradient of expression of Thy-1 mRNA evident around the mitral cell layer. Thy-1 protein, on the other hand, was first detectable 2 days later on a group of mitral cells immediately adjacent the point of entry of the olfactory nerve. The numbers of immunoreactive cells spread, over the next 7 days, to include all mitral cells, those located rostrally and laterally in the bulb being slowest to express Thy-1 protein. Thus there was a spatiotemporal gradient of expression of Thy-1 protein, which was not apparent in the earlier general expression of its mRNA, suggesting that some further inductive signal was required after transcription in order to get effective production of protein. Analysis of the growth of the mitral cell axons in the lateral olfactory tract suggested this signal was related to the cessation of axonogenesis, as Thy-1 immunoreactivity became detectable on these axons only when their expression of the transient epitope detected by the GIO antibody, present on microtubule-associated protein (MAP)lx only during axonal growth, declined.<\/jats:p>\n               <jats:p>For the first week after Thy-1 protein appeared on mitral cells, it was not distributed uniformally on their surface. Immunoreaction was relatively weak on the somatic surface, and the molecule appeared to be entirely excluded from the distal regions of its main dendrite, above the outer plexiform layer. Here the dendrite reaches up to the synaptic glomeruli formed with the incoming olfactory nerve axons. These distal regions of the dendritic shaft became immunoreactive only after the periglomerular cells had first begun to express Thy-1 protein in the glomeruli. Immunolabelling of the somatic membrane then increased, to give the adult pattern of uniform Thy-1 labelling of the neuronal membrane by the end of the second postnatal week. It is suggested that some of the molecular features of Thy-1, and anatomical features of the main bulb, could interact to produce this initial restriction of Thy-1 to particular parts of the mitral cell suface.<\/jats:p>\n               <jats:p>Despite the mitral cells of the accessory olfactory bulb developing earlier than those of the main bulb, both Thy-1 mRNA and protein appeared 5 \u20137 days later on the cells of the accessory bulb. This may be related to the guidance role that the accessory axons are thought to play in respect of the later developing fibres of the main bulb.<\/jats:p>","DOI":"10.1242\/dev.109.4.851","type":"journal-article","created":{"date-parts":[[2021,4,24]],"date-time":"2021-04-24T09:17:26Z","timestamp":1619255846000},"page":"851-864","source":"Crossref","is-referenced-by-count":40,"title":["Expression of the neuronal surface glycoprotein Thy-1 is under post-transcriptional control, and is spatially regulated, in the developing olfactory system"],"prefix":"10.1242","volume":"109","author":[{"given":"G. P.","family":"Xue","sequence":"first","affiliation":[{"name":"1 Norman and Sadie Lee Research Centre, Laboratory of Neurobiology, National Institute for Medical Research, Mill Hill, London NW7 1AA, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. 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