Physiological ROS controls Upd3-dependent modeling of ECM to support cardiac function in Drosophila
Jayati Gera1, Prerna Budakoti1, Meghna Suhag1
1Molecular Cell and Developmental Biology Laboratory, Department of Biological Sciences, Indian Institute of Science Education and Research Mohali, Punjab 140306, India.
Science Advances
|February 18, 2022
Summary
This study reveals a novel ROS-dependent signaling pathway in Drosophila. Elevated reactive oxygen species (ROS) within cells trigger cytokine release, influencing cardiac function and lifespan via extracellular matrix modulation.
Area of Science:
- Cellular biology
- Physiology
- Genetics
Background:
- Reactive oxygen species (ROS) are crucial signaling molecules in biological processes.
- ROS typically act autonomously or signal via diffusion, but novel mechanisms are being explored.
Purpose of the Study:
- To investigate ROS-dependent paracrine signaling without ROS release.
- To elucidate the molecular pathway linking ROS to inter-organ communication and cardiac function.
Main Methods:
- In vivo molecular genetic analyses in Drosophila.
- Examination of signaling cascades involving Ask1, c-Jun N-terminal kinase, and p38.
- Analysis of cytokine Unpaired 3 (Upd3) and extracellular matrix protein Pericardin expression.
Main Results:
- Demonstrated ROS-dependent paracrine signaling independent of ROS release.
- Identified a signaling cascade: ROS → Ask1/JNK/p38 → Upd3.
- Showcased Upd3's role in regulating Pericardin expression in the fat body, impacting cardiac function.
Conclusions:
- Revealed an unexpected inter-organ communication pathway regulated by intracellular ROS.
- Highlighted the role of ROS in modulating cytokine-dependent cardiac extracellular matrix.
- Implications for understanding normal physiology and pathophysiological conditions related to ROS signaling.
