Rickettsiaceae, rickettsia-like endosymbionts, and the origin of mitochondria
- PMID: 11508688
- DOI: 10.1023/a:1010409415723
Rickettsiaceae, rickettsia-like endosymbionts, and the origin of mitochondria
Abstract
Accumulating evolutionary data point to a monophyletic origin of mitochondria from the order Rickettsiales. This large group of obligate intracellular alpha-Proteobacteria includes the family Rickettsiaceae and several rickettsia-like endosymbionts (RLEs). Detailed phylogenetic analysis of small subunit (SSU) rRNA and chaperonin 60 (Cpn60) sequences testify to polyphyly of the Rickettsiales, and consistently indicate a sisterhood of Rickettsiaceae and mitochondria that excludes RLEs. Thus RLEs are considered as the nearest extant relatives of an extinct last common ancestor of mitochondria and rickettsiae. Phylogenetic inferences prompt the following assumptions. (1) Mitochondrial origin has been predisposed by the long-term endosymbiotic relationship between rickettsia-like bacteria and proto-eukaryotes, in which many endosymbiont genes have been lost while some indispensable genes have been transferred to the host genome. (2) The obligate dependence of rickettsiae upon a eukaryotic host rests on the import of proteins encoded by these transferred genes. The nature of a proto-eukaryotic cell still remains elusive. The divergence of Rickettsiaceae and mitochondria based on Cpn60, and the evolutionary history of two aminoacyl-tRNA synthetases favor the hypothesis that it was a chimera created by fusion of an archaebacterium and a eubacterium not long before an endosymbiotic event. These and other, mostly biochemical data suggest that all the mitochondrion-related organelles, i.e., both aerobically and anaerobically respiring mitochondria and hydrogenosomes, have originated from the same RLE, while hydrogenosomal energy metabolism may have a separate origin resulting from a eubacterial fusion partner.
Similar articles
-
Evolutionary relationship of Rickettsiae and mitochondria.FEBS Lett. 2001 Jul 13;501(1):11-8. doi: 10.1016/s0014-5793(01)02618-7. FEBS Lett. 2001. PMID: 11457448
-
[Suggested mitochondrial ancestry of non-mitochondrial ATP/ADP].Mol Biol (Mosk). 2007 Jan-Feb;41(1):59-70. Mol Biol (Mosk). 2007. PMID: 17380892 Russian.
-
[Evolutionary relationship of Rickettsia and eukaryotic mitochondria].Vestn Ross Akad Med Nauk. 2000;(3):3-7. Vestn Ross Akad Med Nauk. 2000. PMID: 10765727 Russian.
-
Mitochondrial connection to the origin of the eukaryotic cell.Eur J Biochem. 2003 Apr;270(8):1599-618. doi: 10.1046/j.1432-1033.2003.03499.x. Eur J Biochem. 2003. PMID: 12694174 Review.
-
Mitochondrial evolution.Science. 1999 Mar 5;283(5407):1476-81. doi: 10.1126/science.283.5407.1476. Science. 1999. PMID: 10066161 Review.
Cited by
-
Role of Mitochondria-Derived Danger Signals Released After Injury in Systemic Inflammation and Sepsis.Antioxid Redox Signal. 2021 Nov 20;35(15):1273-1290. doi: 10.1089/ars.2021.0052. Epub 2021 May 25. Antioxid Redox Signal. 2021. PMID: 33847158 Free PMC article. Review.
-
Evolution of the human mitochondrial ABCB7 [2Fe-2S](GS)4 cluster exporter and the molecular mechanism of an E433K disease-causing mutation.Arch Biochem Biophys. 2021 Jan 15;697:108661. doi: 10.1016/j.abb.2020.108661. Epub 2020 Nov 3. Arch Biochem Biophys. 2021. PMID: 33157103 Free PMC article.
-
"Candidatus Fokinia solitaria", a Novel "Stand-Alone" Symbiotic Lineage of Midichloriaceae (Rickettsiales).PLoS One. 2016 Jan 5;11(1):e0145743. doi: 10.1371/journal.pone.0145743. eCollection 2016. PLoS One. 2016. PMID: 26731731 Free PMC article.
-
Cardiolipin signaling mechanisms: collapse of asymmetry and oxidation.Antioxid Redox Signal. 2015 Jun 20;22(18):1667-80. doi: 10.1089/ars.2014.6219. Epub 2015 Mar 31. Antioxid Redox Signal. 2015. PMID: 25566681 Free PMC article. Review.
-
Mitochondrial stress signaling promotes cellular adaptations.Int J Cell Biol. 2014;2014:156020. doi: 10.1155/2014/156020. Epub 2014 Jan 22. Int J Cell Biol. 2014. PMID: 24587804 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials