Developmental Axon Pruning Requires Destabilization of Cell Adhesion by JNK Signaling

Bavat Bornstein, Eitan Erez Zahavi, Sivan Gelley, Maayan Zoosman, Shiri Penina Yaniv, Ora Fuchs, Ziv Porat, Eran Perlson, Oren Schuldiner*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Developmental axon pruning is essential for normal brain wiring in vertebrates and invertebrates. How axon pruning occurs in vivo is not well understood. In a mosaic loss-of-function screen, we found that Bsk, the Drosophila JNK, is required for axon pruning of mushroom body γ neurons, but not their dendrites. By combining in vivo genetics, biochemistry, and high-resolution microscopy, we demonstrate that the mechanism by which Bsk is required for pruning is through reducing the membrane levels of the adhesion molecule Fasciclin II (FasII), the NCAM ortholog. Conversely, overexpression of FasII is sufficient to inhibit axon pruning. Finally, we show that overexpressing other cell adhesion molecules, together with weak attenuation of JNK signaling, strongly inhibits pruning. Taken together, we have uncovered a novel and unexpected interaction between the JNK pathway and cell adhesion and found that destabilization of cell adhesion is necessary for efficient pruning.

Original languageEnglish
Pages (from-to)926-940
Number of pages15
JournalNeuron
Volume88
Issue number5
DOIs
StatePublished - 2 Dec 2015

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