Patronin governs minus-end-out orientation of dendritic microtubules to promote dendrite pruning in Drosophila.

Yan Wang,Menglong Rui,Shufeng Bu,Fengwei Yu,Quan Tang

doi:10.7554/elife.39964

Yan Wang, Menglong Rui + Show 3 more

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https://doi.org/10.7554/elife.39964

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Abstract

This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that minor issues remain unresolved (see decision letter).

Highlights

In the developing nervous systems, neurons often undergo remodeling events, such as apoptosis, pruning and regrowth, which are pivotal for the refinement of mature neural circuits in both vertebrates and invertebrates (Luo and O’Leary, 2005; Riccomagno and Kolodkin, 2015)
Mutant ddaC neurons derived from patronin RNA interference (RNAi) expression (#1, n = 16, Figure 1C and H) or patroninc9-c5 mutant clones (n = 13, Figure 1D and H) exhibited severe dendrite pruning defects with full penetrance at 16 hr after puparium formation (APF)
The dendrites of patronin RNAi ddaC neurons were largely removed by 32 hr APF (n = 32; Figure 1—figure supplement 1B), presumably due to extensive apoptosis/migration of the dorsal abdominal epidermis, on which neurons arborize their larval dendrites (Williams and Truman, 2005)

Summary

Introduction

In the developing nervous systems, neurons often undergo remodeling events, such as apoptosis, pruning and regrowth, which are pivotal for the refinement of mature neural circuits in both vertebrates and invertebrates (Luo and O’Leary, 2005; Riccomagno and Kolodkin, 2015). We report that MT minus-end-binding protein Patronin plays a crucial role in dendrite pruning in class IV ddaC neurons. The CKK domain is important for Patronin’s function in governing dendrite pruning Both patronin knockdown and overexpression resulted in a drastic decrease of the MT minus-end marker Nod-b-gal and a significant increase of anterograde EB1-GFP comets in proximal ddaC dendrites, indicating that Patronin may stabilize uniform minus-end-out MTs in the dendrites. Attenuation of Klp10A, a kinesin-13 MT depolymerase, in patronin ddaC neurons significantly restored uniform minus-end-out MTs in dendrites and thereby rescued dendrite pruning defects. Our study demonstrates, for the first time, that the MT minus-end-binding protein Patronin orients uniform minus-end-out MT arrays in dendrites to govern dendrite-specific pruning mainly through antagonizing Klp10A activity in Drosophila sensory neurons

Results

Discussion

Materials and methods