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Developmental upregulation of ephrin-B1 silences sema3C/neuropilin-1 signaling during post-crossing navigation of corpus callosum axons

Mire, Erik ORCID: https://orcid.org/0000-0002-6793-0566, Hocine, Melanie, Bazellieres, Elsa, Jungas, Thomas, Davy, Alice, Chauvet, Sophie and Mann, Fanny 2018. Developmental upregulation of ephrin-B1 silences sema3C/neuropilin-1 signaling during post-crossing navigation of corpus callosum axons. Current Biology 28 (11) , pp. 1768-1782. 10.1016/j.cub.2018.04.026

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Abstract

The corpus callosum is the largest commissure in the brain, whose main function is to ensure communication between homotopic regions of the cerebral cortex. During fetal development, corpus callosum axons (CCAs) grow toward and across the brain midline and then away on the contralateral hemisphere to their targets. A particular feature of this circuit, which raises a key developmental question, is that the outgoing trajectory of post-crossing CCAs is mirror-symmetric with the incoming trajectory of pre-crossing axons. Here, we show that post-crossing CCAs switch off their response to axon guidance cues, among which the secreted Semaphorin-3C (Sema3C), that act as attractants for pre-crossing axons on their way to the midline. This change is concomitant with an upregulation of the surface protein Ephrin-B1, which acts in CCAs to inhibit Sema3C signaling via interaction with the Neuropilin-1 (Nrp1) receptor. This silencing activity is independent of Eph receptors and involves a N-glycosylation site (N-139) in the extracellular domain of Ephrin-B1. Together, our results reveal a molecular mechanism, involving interaction between the two unrelated guidance receptors Ephrin-B1 and Nrp1, that is used to control the navigation of post-crossing axons in the corpus callosum

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: Elsevier (Cell Press)
ISSN: 0960-9822
Date of Acceptance: 6 April 2018
Last Modified: 24 Oct 2022 08:36
URI: https://orca.cardiff.ac.uk/id/eprint/118205

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