Ever since Woese and Fox (1977) suggested that the last common ancestor of all life was a precellular incompetent 'progenote' and Van Valen and Maiorana (1980) suggested that eukaryotes evolved from archaebacteria there has been confusion over this issue. Woese and Fox's never remotely tenable idea of the cenancestor as a simple precellular entity has been adequately refuted numerous times by many authors (e.g. Cavalier-Smith 1981, 1987a,b; Pereto et al. 2004) but to this day continues to mislead some who ignore cell biology (Martin and Russell 2003). Since Van Valen and Maiorana (1980) it has been clear that, although some eukaryote genes more closely resemble those of archaebacteria, others are more like those of eubacteria. This has been demonstrated with steadily increasing comprehensiveness and precision with successive advances in DNA sequencing and genomics (Brown and Doolittle 1997; Esser et al. 2004; Golding and Gupta 1995). Too often, genes more similar to those of archaebacteria are called 'archaebacterial'. This is misleading as it begs the question whether archaebacteria are actually ancestors of eukaryotes (i.e. paraphyletic) as Van Valen and Maiorana (1980) suggested, or really their sisters, as ribosomal RNA (rRNA) trees long suggested and I later argued from a cell biological viewpoint (Cavalier-Smith 1987b); if archaebacteria are holophyletic, those genes are neomuran, not archaebacterial. I have strongly opposed the idea of archaebacterial paraphyly (Van Valen and Maiorana 1980) as it entails two changeovers, not just one, in the nature of surface membrane lipids during their history. I proposed the neomuran theory, with the root of the universal tree being in eubacteria, and neomura being holophyletic and derived from posibacterial ancestors, as it involved only one change in membrane lipids and one change in the number of bounding membranes in the history of life and is compatible with the firm evidence from the fossil record that eukaryotes are much younger than eubacteria (probably over 3 times younger; Cavalier-Smith 2006a). In addition, archaebacterial holophyly and eubacterial paraphyly is the only relationship between the three domains compatible not only with the fossil record and a simple interpretation of cell evolution, but also with the mixture of eubacteria-like and archaebacteria-like genes in eukaryotes, without multiplying assumptions devoid of evidence. Despite these major advantages, the theory was usually ignored, until my later discussion (Cavalier-Smith 2002a) that gave greatly increased evidence for polarising the eubacteria/neomuran transition thus, not in reverse. I argued that three gene splits demonstrate archaebacterial holophyly and that the absence of many genes from archaebacteria that are widespread in the other domains was caused by loss in their common ancestor.
As the legend to Fig. 8.1 indicates, the neomuran theory simply explains the observed pattern of gene similarity between eukaryotes and prokaryotes. The theory was recently seriously misrepresented by a claim that it predicts that 'eukaryote nuclear genes should bear greatest overall similarity to their homologues from actinobacteria' (Esser et al. 2004). I have never made that prediction and fail to understand how anyone could deduce it from my theory. I refute it later in this chapter after first discussing the more important issue of how the a-proteobacterium was actually enslaved to make the mitochondrion.
There are no known surviving primitively amitochondrial eukaryotes, making it likely that mitochondrial enslavement took place immediately after the evolution of the protoeukaryote, significantly after the origin of phagocytosis, which provided the mechanism of its ingestion, but possibly during the later stages of perfection of such cenancestral eukaryotic characters as efficient nucleocytoplasmic transport and ciliary motion. It is now highly probable that the cenancestral eukaryote had a centriole and cilium and that there are no primitively non-ciliate eukaryotes (Cavalier-Smith et al. 2004; Kudryavtsev et al. 2005; Richards and Cavalier-Smith 2005). Given also the arguments for a simultaneous origin of nuclei and cilia to generate a unicili-ate eukaryote cenancestor (similar to Phalansterium or Mastigamoeba without mitochondria or mitosomes; Cavalier-Smith 1987b), it is likely that the protoeukaryote also was uniciliate, not a simple amoeba - contrary to early ideas (Whatley et al. 1979). Because the root of the eukaryote tree is between bikonts and unikonts (Richards and Cavalier-Smith 2005; Stechmann and Cavalier Smith 2003), in each of which hydrogenosomes and mitosomes evolved polyphyletically from aerobic cristate mitochondria, the notion that hydrogenosomes are relics of early anaerobic eukaryote evolution is mistaken. All of them evolved from fully aerobic mitochondria, as I first argued (Cavalier-Smith 1987c) when opposing their less parsimonious origin by a separate bacterial enslavement (Whatley et al. 1979). Representatives of every protozoan phylum can be isolated from anaerobic as well as aerobic habitats. The capacity to grow aerobically, microaerophilically, or anaerobically is very widespread and probably was ancestral. Thus, mitochondria probably primitively had considerable potential to become hydrogenosomes in some lineages, or more strictly aerobic in others. As other chapters deal with the secondary polyphyletic origins of hydrogenosomes in detail, here I simply point out that they probably all retain the ancestral mitochondrial protein-import mechanism, despite in most cases having entirely lost the proteobacterial intraorganellar genomes (but not all their transferred genes) hundreds of millions of years ago, testifying to reliability of membrane heredity in general and the evolutionary longevity of their two genetic membranes that, though acquired from a-proteobacteria, became new kinds of genetic membrane by the origins of novel protein-import machinery (Cavalier-Smith 2004b).
Was this article helpful?
For centuries, ever since the legendary Ponce de Leon went searching for the elusive Fountain of Youth, people have been looking for ways to slow down the aging process. Medical science has made great strides in keeping people alive longer by preventing and curing disease, and helping people to live healthier lives. Average life expectancy keeps increasing, and most of us can look forward to the chance to live much longer lives than our ancestors.