Shared evolutionary footprints suggest mitochondrial oxidative damage underlies multiple complex I losses in fungi

Open Biology

Jozef Nosek¹  Miquel Àngel Schikora-Tamarit²  Marina Marcet-Houben²  Toni Gabaldón² 

[1] Department of Biochemistry, Faculty of Natural Sciences, Comenius University in Bratislava, Ilkovičova 6, 842 15 Bratislava, Slovakia;Life Sciences Department, Barcelona Supercomputing Centre (BSC-CNS), Jordi Girona, 29, 08034 Barcelona, Spain;

关键词: phylogenomics;    complex I;    yeast;    oxidative phosphorylation;    oxidative stress;    mitochondria;   

DOI  :  10.1098/rsob.200362

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown