Sequential formation of Drosophila circuit asymmetry via prolonged structural plasticity

TL;DR

This study shows how asymmetry in Drosophila brain circuits develops through interactions of pioneer neurons and structural plasticity.

Contribution

The study reveals a novel mechanism of circuit asymmetry formation via axonal interactions and dynamic adhesion molecule expression in Drosophila.

Findings

Directional asymmetry in Drosophila brain circuits arises from axonal interactions of bilateral pioneer neurons.

Fasciclin 2 expression maintains structural plasticity during axonal remodeling for circuit lateralization.

Reduced circuit asymmetry due to Fasciclin 2 manipulation affects adult brain function.

Abstract

Structural and functional differences between brain hemispheres are a common feature of animal nervous systems with reduced bilateral asymmetry often linked to impaired cognitive performance. How neuronal left-right asymmetry is initiated and integrated into a bilaterally symmetrical ground pattern is poorly understood. Here, we show that the directional asymmetry of a Drosophila central brain circuit originates from axonal interactions of two types of bilateral pioneer neurons. Subsequent recruitment of neighboring neurons into the asymmetric neuropil primordium results in hemisphere-specific microcircuits. Circuit lateralization requires dynamic expression of the cell adhesion molecule Fasciclin 2 to maintain structural plasticity in axonal remodeling. Reduced circuit asymmetry following cell type–specific Fasciclin 2 manipulation affects adult brain function. These results reveal an unexpected degree of developmental plasticity of late-born Drosophila neurons in the formation of a circuit node via the lateralized recruitment of symmetric circuit components.

Late-born neurons in the developing Drosophila brain induce and integrate left-right asymmetry into bilateral neural circuits.

Figures