FGF receptors are required for proper axonal branch targeting in Drosophila

Júnia Vieira Dos Santos,Andrea Terceros,Brian Edwin Chen,Renee Yin Yu

doi:10.1186/s13041-019-0503-y

Júnia Vieira Dos Santos, Andrea Terceros + Show 2 more

Open Access

https://doi.org/10.1186/s13041-019-0503-y

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Journal: Molecular Brain	Publication Date: Oct 24, 2019
Citations: 4	License type: open-access

Affiliation: McGill University Health Centre, McGill University

Abstract

Proper axonal branch growth and targeting are essential for establishing a hard-wired neural circuit. Here, we examined the role of Fibroblast Growth Factor Receptors (FGFRs) in axonal arbor development using loss of function and overexpression genetic analyses within single neurons. We used the invariant synaptic connectivity patterns of Drosophila mechanosensory neurons with their innate cleaning reflex responses as readouts for errors in synaptic targeting and circuit function. FGFR loss of function resulted in a decrease in axonal branch number and lengths, and overexpression of FGFRs resulted in ectopic branches and increased lengths. FGFR mutants produced stereotyped axonal targeting errors. Both loss of function and overexpression of FGFRs within the mechanosensory neuron decreased the animal’s frequency of response to mechanosensory stimulation. Our results indicate that FGFRs promote axonal branch growth and proper branch targeting. Disrupting FGFRs results in miswiring and impaired neural circuit function.

Highlights

Molecular cues allow for axon guidance, target recognition, and synaptogenesis, and along with activity-dependent plasticity, lead to the formation of functioning neural circuits [1]
We sought to determine whether the Btl or Htl Fibroblast Growth Factor (FGF) receptors (FGFRs) were transcribed in mechanosensory neurons
Is the axonal branch growth-promoting function of Btl shared with the other FGFR Htl? We evaluated the axonal arbors of posterior scutellar (pSc) neurons in different Htl mutant animals (Fig. 1h-j)

Summary

Introduction

Molecular cues allow for axon guidance, target recognition, and synaptogenesis, and along with activity-dependent plasticity, lead to the formation of functioning neural circuits [1]. Previous studies have demonstrated the strong axonal growth induction potential of neurotrophic factors such as Fibroblast Growth Factor (FGF) [4, 5] and Nerve Growth Factor (NGF) in cultured cells [6, 7] and animal models [8,9,10]. It is not clear how they might mediate specific axonal targeting decisions that determine neuronal connectivity.

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