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Hirschberg, A.* ; Deng, S.* ; Korostylev, A.* ; Paldy, E.* ; Costa, M.R. ; Worzfeld, T.* ; Vodrazka, P.* ; Wizenmann, A. ; Götz, M. ; Offermanns, S.* ; Kuner, R.*

Gene deletion mutants reveal a role for semaphorin receptors of the plexin-B family in mechanisms underlying corticogenesis.

Mol. Cell. Biol. 30, 764-780 (2010)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Semaphorins and their receptors, plexins, are emerging as key regulators of various aspects of neural and nonneural development. Semaphorin 4D (Sema4D) and B-type plexins demonstrate distinct expression patterns over critical time windows during the development of the murine neocortex. Here, analysis of mice genetically lacking plexin-B1 or plexin-B2 revealed the significance of Sema4D-plexin-B signaling in cortical development. Deficiency of plexin-B2 resulted in abnormal cortical layering and defective migration and differentiation of several subtypes of cortical neurons, including Cajal-Retzius cells, GABAergic interneurons, and principal cells in vivo. In contrast, a lack of plexin-B1 did not impact on cortical development in vivo. In various ex vivo assays on embryonic forebrain, Sema4D enhanced the radial and tangential migration of developing neurons in a plexin-B2-dependent manner. These results suggest that Sema4D-plexin-B2 interactions regulate mechanisms underlying cell specification, differentiation, and migration during corticogenesis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Radial glial-cells; Central-nervous-system; Cortical interneurons; Nuclear antigen; Cycle analysis; Migration; Neurons; Growth; RHO; Proliferation
ISSN (print) / ISBN 0270-7306
e-ISSN 1098-5549
Quellenangaben Band: 30, Heft: 3, Seiten: 764-780 Artikelnummer: , Supplement: ,
Verlag American Society for Microbiology (ASM)
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed