Neuron tracing and quantitative analyses of dendritic architecture reveal symmetrical three-way-junctions and phenotypes of git-1 in C. elegans

Abstract

Complex dendritic trees are a distinctive feature of neurons. Alterations to dendritic morphology are associated with developmental, behavioral and neurodegenerative changes. The highly-arborized PVD neuron of C. elegans serves as a model to study dendritic patterning; however, quantitative, objective and automated analyses of PVD morphology are missing. Here, we present a method for neuronal feature extraction, based on deep-learning and fitting algorithms. The extracted neuronal architecture is represented by a database of structural elements for abstracted analysis. We obtain excellent automatic tracing of PVD trees and uncover that dendritic junctions are unevenly distributed. Surprisingly, these junctions are three-way-symmetrical on average, while dendritic processes are arranged orthogonally. We quantify the effect of mutation in git-1, a regulator of dendritic spine formation, on PVD morphology and discover a localized reduction in junctions. Our findings shed new light on PVD architecture, demonstrating the effectiveness of our objective analyses of dendritic morphology and suggest molecular control mechanisms.

The reverse transcriptase inhibitor 3TC protects against age‐related cognitive dysfunction

“…Based on these observations, we used a model organism to determine whether 3TC may directly protect aging neurons. C. elegans PVD neurons serve as a model to study how dendritic morphology changes with aging (Yuval et al, 2021 ); here, we showed that the PVD neuron degenerates with aging, consistent with other reports that have linked this degeneration with immune sensor activation (Lezi et al, 2018 ), but that 3TC protects against this degeneration and preserves dendritic structure. Dendrites also degenerate with aging in most mammals (Furusawa & Emoto, 2021 ), and therefore, our results could suggest a neuron‐specific mechanism by which 3TC may improve cognitive function in mice.…”

Caenorhabditis elegans neuropeptide NLP-27 enhances neurodegeneration and paralysis in an opioid-like manner during fungal infection

“…The neurons are located between the hypodermis and its basement membrane. 38 The PVD neurons form a network of branches that envelop the body and tail of the nematode ( Figure 5 A). To investigate if A. flagrans infection can cause PVD neurodegeneration, the NC1686 C. elegans strain, where PVD neurons are visualized by GFP, was used in a fungal infection assay ( Figure 5 ).…”