Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jul 29;8:622. doi: 10.3389/fcell.2020.00622

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2020 Sheel, Shao, Brown, Johnson, Hamilton, Sun, Oppenheimer, Smith, Visconti, Markstein, Bigelow and Schwartz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Model for ISM cell death. On day 17 of pupal–adult development, the circulating levels of 20E decline below a threshold that triggers the expression of both the Eclosion Hormone Receptor (EHR) and Acheron. Acheron binds to and stabilizes the pro-death protein BBH1, which then accumulates. A further decline of 20E on day 18 triggers the release of eclosion hormone, which binds to the EHR and drives the production of cGMP, the conversion of inactive protein kinase G (PKGi) into PKG active (PKGa), and Acheron phosphorylation, which leads to its degradation. This liberates BBH1, which then induces the release and degradation of cytochrome c from mitochondria and the subsequent non-apoptotic death of the muscles. (Solid lines denote events that have been demonstrated experimentally, while dashed lines have not been formally tested).