FEIT Research Project Database

The powerhouse of the cell: defining the governing laws of mitochondrial motion


Project Leader: Vijayaraghavan Rajagopal
Collaborators: Senthil Arumugam (Monash)
Primary Contact: Vijayaraghavan Rajagopal (vijay.rajagopal@unimelb.edu.au)
Keywords: cardiovascular disease; finite element modelling; mathematical modelling; Synthetic Biology
Disciplines: Biomedical Engineering
Domains:

Mitochondria are organelles inside cells that produce the energy needed to sustain life. Proper mitochondria organisation and function is therefore critical for health. Dysfunction and disorganisation of mitochondria within cells are associated with many diseases in the body including parkinsons disease, heart failure and more. But we are yet to understand fundamentally how mitochondria organisation and dynamics regulate energy production and consumption. This project aims to uncover the fundamental principles that govern mitochondria organisation, their movements and their impact on energy supply and demand within cells. These principles will transform our understanding of how cells use energy. The principles and computational modelling tools we develop will be useful to identify new drug targets related to mitochondria form and function for treatment of a variety of mitochondria related diseases in the body. A particular application focus in our group is the heart. 

We are seeking applications from outstanding graduates to fill several PhD positions related to imaging and modelling mitochondria dynamics and bioenergetics. Examples of techniques and theories that we will use and advance in this multi-disciplinary project include advanced microscopy, image processing (with and without deep learning), agent-based modelling, finite element modelling, computational systems biology and thermodynamics.

Further information: https://www.biorxiv.org/content/10.1101/2020.09.21.307306v1.abstract https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1006640

Simulation prediction of mitochondrial membrane potential distribution within a cardiomyocyte affected by hypoxia
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