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© 2015, Auer et al. This work is licensed under the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/3.0/ ) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

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.

DOI: http://dx.doi.org/10.7554/eLife.05061.001

Details

Title
Deletion of a kinesin I motor unmasks a mechanism of homeostatic branching control by neurotrophin-3
Author
Auer, Thomas O; Tong, Xiao; Bercier Valerie; Gebhardt Christoph; Duroure Karine; Jean-Paul, Concordet; Wyart Claire; Suster Maximiliano; Kawakami Koichi; Wittbrodt Joachim; Baier Herwig; Filippo, Del Bene
University/institution
U.S. National Institutes of Health/National Library of Medicine
Publication year
2015
Publication date
2015
Publisher
eLife Sciences Publications Ltd.
e-ISSN
2050084X
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1966514442
Copyright
© 2015, Auer et al. This work is licensed under the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/3.0/ ) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.