Francois Singh

Dr. Francois Singh obtained his PhD in Cellular and molecular aspects of Biology in 2016 from the University of Strasbourg (France). His PhD project was realised in co-direction between the Clinical Pharmacology and Toxicology lab of Professor Stephan Krähenbühl at the University of Basel (Switzerland) and the EA3072: Mitochondria, Oxidative Stress and Muscular Protection Lab of Professor Bernard Geny at the University of Strasbourg (France). He investigated the role of mitochondrial adaptations in statin-induced myotoxicity, focusing on the opposite effect of statins in glycolytic and in oxidative muscles. During that time, he also taught medical students at the University hospital of Strasbourg Physiology, as well as Toxicology students at the Department of Pharmaceutical Sciences in Basel.

In 2017, he joined the lab of Professor Ian Ganley as a postdoctoral research assistant at the MRC-Protein Phosphorylation and ubiquitylation unit, University of Dundee, United Kingdom, in collaboration with GlaxoSmithKline. His project investigated the physiological role of pathogenic mutations involved in Parkinson’s disease on mitophagy and general autophagy in vivo. His work provided the first in vivo evidence that pathogenic LRRK2 directly impairs basal mitophagy and demonstrated that pharmacological inhibition of LRRK2 is a rational mitophagy-rescue approach and potential PD therapy.

In 2023, Francois became Assistant Professor at the department of Physiology, School of Health Sciences, University of Iceland.

Mitochondria are the cell’s main actors in charge of not only energy production, but are also involved in calcium homeostasis regulation, the production and scavenging of free radicals, intracellular pH regulation, heme biosynthesis, lipid biosynthesis and metabolism, ubiquinol and Fe-S centres biosynthesis, steroid hormones production, and in controlling the programmed cell death. These vital functions are dependent on mitochondrial content and quality. Mitochondria are dynamic organelles that can adjust to the cell’s changing needs via a delicate balance between the production of new mitochondria through biogenesis, and their elimination via mitophagy, the autophagy of the mitochondria.

My aim is to investigate how mitochondrial homeostasis is regulated basally, as well as in pathological contexts. 

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