This PhD project investigates how age-related alterations in reactive oxygen species (ROS) affect the activity of redox-sensitive TRP ion channels. Using live-cell fluorescence microscopy with organelle-targeted biosensors alongside molecular biology approaches, it will map ROS-TRP interactions and the downstream pathways they engage during aging. Mechanistic findings will be linked to organismal outcomes in C. elegans and then tested for conservation in mammalian cellular aging models.
Project Details
Background:
Reactive oxygen species (ROS) are central regulators of cellular signaling but become increasingly dysregulated during aging, contributing to functional decline across tissues. In parallel, transient receptor potential (TRP) channels constitute a highly conserved superfamily of cation channels that control ion homeostasis, excitability, and stress responses. Importantly, several TRP family members can respond to ROS, suggesting that TRP channels may act as redox-sensitive signal hubs that translate oxidative stress into downstream physiological programs. This is particularly relevant in aging, where elevated ROS levels coincide with progressive deterioration of subcellular integrity, including changes in mitochondrial structure, redox balance, and stress resilience.
Hypothesis and Objectives:
We hypothesize that age-associated ROS elevation modifies the activity of redox-sensitive TRP channels, thereby perturbing ion homeostasis and stress-response signaling and ultimately contributing to reduced organismal fitness and longevity. To test this hypothesis, this Ph.D. project will utilize Caenorhabditis elegans (C. elegans) and mammalian cellular aging models to molecularly and functionally characterize ROS-sensitive TRP channels during aging and to identify the downstream signaling cascades that connect ROS-TRP interactions to stress resistance and aging pathways.
Methodology:
The candidate will combine live-cell fluorescence microscopy using organelle-targeted biosensors to define TRP channel activity and its modulation by ROS, complemented by molecular biology approaches to resolve downstream pathway engagement. In C. elegans, these mechanistic insights will be linked to organismal phenotypes, including locomotion, stress resilience, and lifespan. At the same time, key mechanisms will be tested for conservation in mammalian aging models.
References
Please familiarize yourself with our publications via PubMed Madreiter-Sokolowski
People Involved
Primary supervisor: Corina Madreiter-Sokolowski
Collaborators: