PuSH - Publikationsserver des Helmholtz Zentrums München: Loss of Npn1 from motor neurons causes postnatal deficits independent from Sema3A signaling.

Navigation

Startseite

English

Recherche

Erweiterte Suche

Durchblättern nach ...

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Erscheinungsjahr

Publikationen im Überblick

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmbrecht, M.S. ; Soellner, H. ; Truckenbrodt, A.M. ; Sundermeier, J. ; Cohrs, C.M. ; Hans, W. ; Hrabě de Angelis, M. ; Feuchtinger, A. ; Aichler, M. ; Fouad, K.* ; Huber, A.B.

Loss of Npn1 from motor neurons causes postnatal deficits independent from Sema3A signaling.

Dev. Biol. 399, 2-14 (2015)

DOI

PMC

Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

Abstract
Metriken
Zusatzinfos

The correct wiring of neuronal circuits is of crucial importance for the function of the vertebrate nervous system. Guidance cues like the neuropilin receptors (Npn) and their ligands, the semaphorins (Sema) provide a tight spatiotemporal control of sensory and motor axon growth and guidance. Among this family of guidance partners the Sema3A-Npn1 interaction has been shown to be of great importance, since defective signaling leads to wiring deficits and defasciculation. For the embryonic stage these defects have been well described, however, also after birth the organism can adapt to new challenges by compensational mechanisms. Therefore, we used the mouse lines Olig2-Cre;Npn1(cond) and Npn1(Sema-) to investigate how postnatal organisms cope with the loss of Npn1 selectively from motor neurons or a systemic dysfunctional Sema3A-Npn1 signaling in the entire organism, respectively. While in Olig2-Cre(+);Npn1(cond-/-) mice clear anatomical deficits in paw posturing, bone structure, as well as muscle and nerve composition became evident, Npn1(Sema-) mutants appeared anatomically normal. Furthermore, Olig2-Cre(+);Npn1(cond) mutants revealed a dysfunctional extensor muscle innervation after single-train stimulation of the N.radial. Interestingly, these mice did not show obvious deficits in voluntary locomotion, however, skilled motor function was affected. In contrast, Npn1(Sema-) mutants were less affected in all behavioral tests and able to improve their performance over time. Our data suggest that loss of Sema3A-Npn1 signaling is not the only cause for the observed deficits in Olig2-Cre(+);Npn1(cond-/-) mice and that additional, yet unknown binding partners for Npn1 may be involved that allow Npn1(Sema-) mutants to compensate for their developmental deficits.

Altmetric

Weitere Metriken?

[➜Einloggen]