A model of muscle atrophy based on live microscopy of muscle remodelling in Drosophila metamorphosis

Royal Society Open Science
KuleeshaMartin Wasser

Abstract

Genes controlling muscle size and survival play important roles in muscle wasting diseases. In Drosophila melanogaster metamorphosis, larval abdominal muscles undergo two developmental fates. While a doomed population is eliminated by cell death, another persistent group is remodelled and survives into adulthood. To identify and characterize genes involved in the development of remodelled muscles, we devised a workflow consisting of in vivo imaging, targeted gene perturbation and quantitative image analysis. We show that inhibition of TOR signalling and activation of autophagy promote developmental muscle atrophy in early, while TOR and yorkie activation are required for muscle growth in late pupation. We discovered changes in the localization of myonuclei during remodelling that involve anti-polar migration leading to central clustering followed by polar migration resulting in localization along the midline. We demonstrate that the Cathepsin L orthologue Cp1 is required for myonuclear clustering in mid, while autophagy contributes to central positioning of nuclei in late metamorphosis. In conclusion, studying muscle remodelling in metamorphosis can provide new insights into the cell biology of muscle wasting.

References

May 5, 2016·BMC Developmental Biology· KuleeshaMartin Wasser
Oct 9, 2019·The Journal of Cell Biology·Christoph SchaubManfred Frasch
Dec 3, 2020·Molecular Biology Reports·Madhavi DubeyHena Firdaus

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Related Concepts

Establishment and Maintenance of Localization
In Vivo
Trimethylamine-N-oxide Reductase (Cytochrome C) Activity
Midline (Qualifier Value)
Size
TOR Signaling Cascade
Genes
Drosophila
Cell Nucleus
Wasting Syndrome

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