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Updated: Dec 10, 2025

Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle

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Published on: October 26, 2017

Acheron/Larp6 Is a Survival Protein That Protects Skeletal Muscle From Programmed Cell Death During Development.

Ankur Sheel^1,2, Rong Shao^1,2,3, Christine Brown¹

¹Department of Biology, University of Massachusetts Amherst, Amherst, MA, United States.

Frontiers in Cell and Developmental Biology

|August 28, 2020

Summary

Programmed cell death (PCD) in moth muscles involves the survival protein Acheron, which is degraded upon eclosion hormone signaling, initiating cell death. This pathway is conserved in fruit flies and relevant to human cancers.

Keywords:

BAD BBH1 Drosophila Manduca sexta apoptosis autophagy cytochrome c intersegmental muscle

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Published on: September 18, 2019

Area of Science:

Developmental Biology
Cell Biology
Molecular Biology

Background:

Programmed cell death (PCD) is crucial for development, but the signaling pathways are not fully understood.
Hormonally controlled cell death in moth intersegmental muscles (ISMs) requires new gene expression, yet the specific pathway remains elusive.

Purpose of the Study:

To elucidate the signal transduction pathway linking hormone action to cell death in Manduca sexta ISMs.
To identify key proteins involved in the hormonally regulated death of ISMs during metamorphosis.

Main Methods:

Quantification of Acheron/LARP6 mRNA levels during moth metamorphosis.
Analysis of Acheron protein phosphorylation and degradation in response to Eclosion Hormone (EH).
Investigation of the interaction between Acheron and BBH1 using RNA interference (RNAi) in Drosophila.

Main Results:

Acheron/LARP6 mRNA expression increased dramatically as ISMs committed to die.
Acheron acts as a survival protein, being phosphorylated and degraded by EH, which liberates BBH1.
BBH1 accumulation and subsequent cytochrome c release precede cell death, a process confirmed by RNAi in Drosophila.

Conclusions:

A novel pathway involving Acheron and BBH1 mediates EH-induced PCD in moth ISMs.
Acheron functions as a survival factor, while its degradation triggers cell death.
The Acheron-BBH1 pathway's conservation and Acheron's role in human cancers suggest therapeutic potential.