In addition to their repeated secondary diversification to form anaerobic hydrogenosomes and mitosomes, there would have been many adaptive specialisations of aerobic mitochondria unique to particular lineages. We know far too little about mitochondrial function in protists to be able to reconstruct them. For example, although some ciliates can use nitrate as a terminal electron acceptor (Finlay et al. 1983), we do not know if this is an ancestral or a derived trait. The fact that animals do P-oxidation of lipids in mitochondria as well as peroxisomes may be a derived trait, as plants and fungi seem not to. However, evolutionary losses can confound such conclusions when taxon sampling is sparse. It is likely that the origin of plastids had repercussions on mitochondria through the origin of photorespiration that involves both organelles plus peroxisomes. Protists vary greatly in their preferences for different oxygen concentrations and are likely to have contrasting adaptations to exploit natural redox gradients. Such adaptations probably mainly involve nuclear-coded genes, often perhaps of host origin. The great diversity across lineages in which protein genes were retained in the mitochondrial genome (Gray et al. 2004) is likely mainly to reflect historical accidents in successfully overcoming the graded difficulty of retargeting their encoded proteins rather than adaptive factors. Lineages that by chance evolved transfer RNA (tRNA) import mechanisms (Bhattacharyya et al. 2003) could lose mitochondrial tRNA genes. Other differences among lineages might not be adaptive. For example, most lineages retained the proteobacterial FtsZ for dividing their IM (Kiefel et al. 2004; Miyagishima et al. 2004; Osteryoung and Nunnari 2003), but opisthokonts lost it, presumably after evolving an extra dynamin ring.
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