Journal
OPEN BIOLOGY
Volume 11, Issue 4, Pages -Publisher
ROYAL SOC
DOI: 10.1098/rsob.200362
Keywords
phylogenomics; complex I; yeast; oxidative phosphorylation; oxidative stress; mitochondria
Categories
Funding
- Spanish Ministry of Science and Innovation [PGC2018-099921-B-I00]
- CERCA Programme/Generalitat de Catalunya
- Catalan Research Agency (AGAUR) [SGR423]
- European Union's Horizon 2020 research [ERC-2016-724173]
- Instituto de Salud Carlos III-Instituto Nacional de Bioinformatica [PT17/0009/0023-ISCIII-SGEFI/ERDF]
- 'Caixa' Foundation [LCF/BQ/DR19/11740023]
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By using a comparative genomics approach, eight independent events of mitochondrial complex I loss across eukaryotes were identified, six of which occurred in fungal lineages. It is hypothesized that the loss of complex I in fungi may be induced by previously acquired compensatory mechanisms and exposure to environmental triggers of oxidative stress.
Oxidative phosphorylation is among the most conserved mitochondrial pathways. However, one of the cornerstones of this pathway, the multi-protein complex NADH : ubiquinone oxidoreductase (complex I) has been lost multiple independent times in diverse eukaryotic lineages. The causes and consequences of these convergent losses remain poorly understood. Here, we used a comparative genomics approach to reconstruct evolutionary paths leading to complex I loss and infer possible evolutionary scenarios. By mining available mitochondrial and nuclear genomes, we identified eight independent events of mitochondrial complex I loss across eukaryotes, of which six occurred in fungal lineages. We focused on three recent loss events that affect closely related fungal species, and inferred genomic changes convergently associated with complex I loss. Based on these results, we predict novel complex I functional partners and relate the loss of complex I with the presence of increased mitochondrial antioxidants, higher fermentative capabilities, duplications of alternative dehydrogenases, loss of alternative oxidases and adaptation to antifungal compounds. To explain these findings, we hypothesize that a combination of previously acquired compensatory mechanisms and exposure to environmental triggers of oxidative stress (such as hypoxia and/or toxic chemicals) induced complex I loss in fungi.
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