MIPCHIP · Mitochondrial protein characterisation and interaction prediction
FP6 — Marie Curie Actions (Human Resources and Mobility)
- Duration
- 2006-10-18 → 2008-05-17
- EU contribution
- €159,046
- Participants
- 1
- Scheme
- EIF
Lines connect the coordinator with its partners.
Results in brief
Final Activity Report Summary - MIPCHIP (Mitochondrial protein characterisation and interaction prediction)
The canonical function of mitochondria in most textbooks is oxidative phosphorylation. However, many parasitic eukaryotes live in low oxygen environments where this cannot occur, yet they still keep their mitochondria, although they are often called mitosomes or hydrogenosomes. To understand why we carried out an exhaustive computational analysis of the genomes of a sample of eukaryotes that live under different conditions. The results, organised into a relational database, have provided the clearest picture yet of how mitochondria evolve under contrasting host lifestyles. From the results it is clear that reductive evolution, whereby organelles have lost biochemical pathways or structural proteins, has occurred repeatedly and independently for different eukaryotes. As predicted, the genes for oxidative phosphorylation are commonly lost. What was surprising, however, is just how few proteins are strongly conserved. For example, the only metabolic pathway that appears to be conserved on all genomes, is one for the biosynthesis of iron-sulphur clusters. This is already known to be an essential feature of yeast mitochondria but our work shows that it may be a fundamental metabolic reason for why all eukaryotic cells have kept mitochondria. Experimental work is underway to test this hypothesis.
Data: CORDIS, © European Union
Project objective
Recent work suggests that all eukaryotes, irrespective of their lifestyle, anaerobic or parasitic, contain an organelle derived from the mitochondrion a mitochondrial homologue, posing the question is there a common conserved function shared by all mitochondrial homologues that makes them vital for the eukaryotic cell?I will use an innovative comparative bioinformatics approach to identify the cohort of mitochondrial proteins conserved among genomes of diverse parasitic and anaerobic eukaryotes with mitochondrial homologues of different sorts (including hydrogenosomes and mitosomes), and contrast these with the well-characterized proteomes of classic aerobic mitochondria from model organisms.I will also investigate how these proteins might potentially interact and thus infer a mitochondrial functional interactome. These analyses will identify the best candidates for a common essential function (if one indeed exists) for the mitochondrial organelle under diverse living conditions, but will also illustrate the variability of this apparently vital eukaryotic organelle.I will do this work at Newcastle University in the laboratory of Prof. Martin Embley, an expert on mitochondrial homologues of parasitic protozoa. My skills in bioinformatics complement those of Prof. Embley and his collaborators ensuring an excellent synergy and training environment and, through collaboration with researchers in Prof Embleys lab, a unique opportunity to use computational biology to direct focused cell biology.My project is innovative and original and addresses major EU concerns: investigating the functions of organelles of important human parasites addresses a specific goal of EU priority Advanced Genomics and its applications for Health (OJL294, 29.10.02). My project will also provide baseline data for inferring potential minimal functions and structure of mitochondria generally; a Life Sciences Priority (LSH-2003-1.2.2-3).
Original text from CORDIS.
Participants
- UNIVERSITY OF NEWCASTLE UPON TYNE · NEWCASTLE UPON TYNECoordinatorUnited Kingdom
Links
Data: CORDIS, © European Union