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Muscle and epidermal contributions of the structural protein β-spectrin promote hypergravity-induced motor neuron axon defects in C. elegans.

Abstract：

:Biology is adapted to Earth's gravity force, and the long-term effects of varying gravity on the development of animals is unclear. Previously, we reported that high gravity, called hypergravity, increases defects in the development of motor neuron axons in the nematode Caenorhabditis elegans. Here, we show that a mutation in the unc-70 gene that encodes the cytoskeletal β-spectrin protein suppresses hypergravity-induced axon defects. UNC-70 expression is required in both muscle and epidermis to promote the axon defects in high gravity. We reveal that the location of axon defects is correlated to the size of the muscle cell that the axon traverses. We also show that mutations that compromise key proteins of hemidesmosomal structures suppress hypergravity-induced axon defects. These hemidesmosomal structures play a crucial role in coupling mechanical force between the muscle, epidermis and the external cuticle. We speculate a model in which the rigid organization of muscle, epidermal and cuticular layers under high gravity pressure compresses the narrow axon migration pathways in the extracellular matrix hindering proper axon pathfinding of motor neurons.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Kalichamy SS,Alcantara AV Jr,Kim BS,Park J,Yoon KH,Lee JI

doi

10.1038/s41598-020-78414-y

subject

Has Abstract

pub_date

2020-12-03 00:00:00

pages

21214

issue

1

issn

2045-2322

pii

10.1038/s41598-020-78414-y

journal_volume

10

pub_type

杂志文章

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