Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Deletion of a kinesin I motor unmasks a mechanism of homeostatic branching control by neurotrophin-3

MPG-Autoren
/persons/resource/persons39224

Baier,  Herwig
Department: Genes-Circuits-Behavior / Baier, MPI of Neurobiology, Max Planck Society;

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)

elife05061.pdf
(beliebiger Volltext), 5MB

Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Auer, T. O., Xiao, T., Bercier, V., Gebhardt, C., Duroure, K., Concordet, J.-P., et al. (2015). Deletion of a kinesin I motor unmasks a mechanism of homeostatic branching control by neurotrophin-3. ELIFE, 4: e05061. doi:10.7554/eLife.05061.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0029-7726-A
Zusammenfassung
Development and function of highly polarized cells such as neurons depend on microtubule-associated intracellular transport, but little is known about contributions of specific molecular motors to the establishment of synaptic connections. In this study, we investigated the function of the Kinesin I heavy chain Kif5aa during retinotectal circuit formation in zebrafish. Targeted disruption of Kif5aa does not affect retinal ganglion cell differentiation, and retinal axons reach their topographically correct targets in the tectum, albeit with a delay. In vivo dynamic imaging showed that anterograde transport of mitochondria is impaired, as is synaptic transmission. Strikingly, disruption of presynaptic activity elicits upregulation of Neurotrophin-3 (Ntf3) in postsynaptic tectal cells. This in turn promotes exuberant branching of retinal axons by signaling through the TrkC receptor (Ntrk3). Thus, our study has uncovered an activity-dependent, retrograde signaling pathway that homeostatically controls axonal branching.