Active Cells, Biochemistry & Physiology Genetics & Molecular Biology

Mitochondrial cell biology: Understanding the molecular mechanisms and functions of mitochondrial dynamics and membrane contact sites

Funder MRC (part of UKRI)
Recipient organisation University of Cambridge
Funding £3.2M
Period Mar 2022 — Mar 2027

In plain English

AI plain-English summary

Mitochondria inside our cells constantly pinch apart and fuse back together, reshaping their network like a living electrical grid. This reshaping is not random—it controls how mitochondria work, how they talk to other parts of the cell, and whether a cell lives or dies. When these processes go wrong, they have been linked to human diseases, but the specific molecular machinery that drives them remains largely unknown. This project aims to identify the proteins that physically remodel mitochondrial membranes and manage the contact points where mitochondria exchange materials with other organelles. If successful, this work will reveal fundamental mechanisms of how cells maintain health and make decisions about their own survival. Understanding how mitochondrial remodelling governs the release of mitochondrial DNA into the cell—a trigger for inflammation—could eventually point toward new targets for treating metabolic and inflammatory diseases. This is primarily fundamental cell biology: it builds the molecular map of a process that underpins many disease states, rather than delivering an immediate therapy. Past discoveries in mitochondrial dynamics have already reshaped our understanding of neurodegeneration and ageing, and this work extends that foundation.

View original technical description
Mitochondria form a dynamic and connected network, which is constantly remodelled by cycles of membrane fission and fusion. These dynamic transitions are not only required to ensure a proper mitochondrial function but also to respond to cellular needs and adapt to the metabolic state of the cell. To execute cellular functions, mitochondria also establish membrane contact sites with other organelles, including the endoplasmic reticulum, peroxisomes and lysosomes. These organelle membrane contact sites are hotspots for metabolites flux and tightly regulate mitochondrial architecture. While defects in mitochondrial morphology or contact sites have been associated with human diseases, the molecular mechanisms linking mitochondrial membrane remodelling to cell fate decisions are poorly understood. The Prudent group focusses on understanding the mechanisms regulating membrane dynamics and remodelling, how they influence cellular functions and govern cell fate decisions. In our first research aim, we employ state-of-the-art to identify and functionally characterise new proteins regulating mitochondrial morphology and mitochondria-organelle contact sites, and how they govern cell fate decisions. Our second aim of research is to elucidate how mitochondrial membrane remodelling regulates mitochondrial (mt)DNA quality control and modulates cytosolic mtDNA release driving inflammation to control cellular homeostasis.

View the original record at the funder ↗

Researchers

Julien Prudent (Principal Investigator)

Related Research

Grants with similar aims, by meaning.

Investigation of the function of the ER/mitochondria contact sites in cell physiology and disease
Lipid mediated organelle-crosstalk controls cell-fate and function
Role of calcium fluxes in mitochondrial dynamics
Molecular determinants of cardiolipin signalling in mitochondria
Elucidating how inner mitochondrial membrane remodeling regulates mtDNA quality control

Original classification

Intramural

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