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Hofstatter, Paulo G., Alexander K. Tice, Seungho Kang, Matthew W. Brown i Daniel J. G. Lahr. "Evolution of bacterial recombinase A ( recA ) in eukaryotes explained by addition of genomic data of key microbial lineages". Proceedings of the Royal Society B: Biological Sciences 283, nr 1840 (12.10.2016): 20161453. http://dx.doi.org/10.1098/rspb.2016.1453.
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Recombinase enzymes promote DNA repair by homologous recombination. The genes that encode them are ancestral to life, occurring in all known dominions: viruses, Eubacteria, Archaea and Eukaryota. Bacterial recombinases are also present in viruses and eukaryotic groups (supergroups), presumably via ancestral events of lateral gene transfer. The eukaryotic recA genes have two distinct origins (mitochondrial and plastidial), whose acquisition by eukaryotes was possible via primary (bacteria–eukaryote) and/or secondary (eukaryote–eukaryote) endosymbiotic gene transfers (EGTs). Here we present a comprehensive phylogenetic analysis of the recA genealogy, with substantially increased taxonomic sampling in the bacteria, viruses, eukaryotes and a special focus on the key eukaryotic supergroup Amoebozoa, earlier represented only by Dictyostelium . We demonstrate that several major eukaryotic lineages have lost the bacterial recombinases (including Opisthokonta and Excavata), whereas others have retained them (Amoebozoa, Archaeplastida and the SAR-supergroups). When absent, the bacterial recA homologues may have been lost entirely (secondary loss of canonical mitochondria) or replaced by other eukaryotic recombinases. RecA proteins have a transit peptide for organellar import, where they act. The reconstruction of the RecA phylogeny with its EGT events presented here retells the intertwined evolutionary history of eukaryotes and bacteria, while further illuminating the events of endosymbiosis in eukaryotes by expanding the collection of widespread genes that provide insight to this deep history.
2
Martin Embley, T. "Multiple secondary origins of the anaerobic lifestyle in eukaryotes". Philosophical Transactions of the Royal Society B: Biological Sciences 361, nr 1470 (3.05.2006): 1055–67. http://dx.doi.org/10.1098/rstb.2006.1844.
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Classical ideas for early eukaryotic evolution often posited a period of anaerobic evolution producing a nucleated phagocytic cell to engulf the mitochondrial endosymbiont, whose presence allowed the host to colonize emerging aerobic environments. This idea was given credence by the existence of contemporary anaerobic eukaryotes that were thought to primitively lack mitochondria, thus providing examples of the type of host cell needed. However, the groups key to this hypothesis have now been shown to contain previously overlooked mitochondrial homologues called hydrogenosomes or mitosomes; organelles that share common ancestry with mitochondria but which do not carry out aerobic respiration. Mapping these data on the unfolding eukaryotic tree reveals that secondary adaptation to anaerobic habitats is a reoccurring theme among eukaryotes. The apparent ubiquity of mitochondrial homologues bears testament to the importance of the mitochondrial endosymbiosis, perhaps as a founding event, in eukaryotic evolution. Comparative study of different mitochondrial homologues is needed to determine their fundamental importance for contemporary eukaryotic cells.
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Martin, William F., Sriram Garg i Verena Zimorski. "Endosymbiotic theories for eukaryote origin". Philosophical Transactions of the Royal Society B: Biological Sciences 370, nr 1678 (26.09.2015): 20140330. http://dx.doi.org/10.1098/rstb.2014.0330.
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For over 100 years, endosymbiotic theories have figured in thoughts about the differences between prokaryotic and eukaryotic cells. More than 20 different versions of endosymbiotic theory have been presented in the literature to explain the origin of eukaryotes and their mitochondria. Very few of those models account for eukaryotic anaerobes. The role of energy and the energetic constraints that prokaryotic cell organization placed on evolutionary innovation in cell history has recently come to bear on endosymbiotic theory. Only cells that possessed mitochondria had the bioenergetic means to attain eukaryotic cell complexity, which is why there are no true intermediates in the prokaryote-to-eukaryote transition. Current versions of endosymbiotic theory have it that the host was an archaeon (an archaebacterium), not a eukaryote. Hence the evolutionary history and biology of archaea increasingly comes to bear on eukaryotic origins, more than ever before. Here, we have compiled a survey of endosymbiotic theories for the origin of eukaryotes and mitochondria, and for the origin of the eukaryotic nucleus, summarizing the essentials of each and contrasting some of their predictions to the observations. A new aspect of endosymbiosis in eukaryote evolution comes into focus from these considerations: the host for the origin of plastids was a facultative anaerobe.
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Hjort, Karin, Alina V. Goldberg, Anastasios D. Tsaousis, Robert P. Hirt i T. Martin Embley. "Diversity and reductive evolution of mitochondria among microbial eukaryotes". Philosophical Transactions of the Royal Society B: Biological Sciences 365, nr 1541 (12.03.2010): 713–27. http://dx.doi.org/10.1098/rstb.2009.0224.
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All extant eukaryotes are now considered to possess mitochondria in one form or another. Many parasites or anaerobic protists have highly reduced versions of mitochondria, which have generally lost their genome and the capacity to generate ATP through oxidative phosphorylation. These organelles have been called hydrogenosomes, when they make hydrogen, or remnant mitochondria or mitosomes when their functions were cryptic. More recently, organelles with features blurring the distinction between mitochondria, hydrogenosomes and mitosomes have been identified. These organelles have retained a mitochondrial genome and include the mitochondrial-like organelle of Blastocystis and the hydrogenosome of the anaerobic ciliate Nyctotherus . Studying eukaryotic diversity from the perspective of their mitochondrial variants has yielded important insights into eukaryote molecular cell biology and evolution. These investigations are contributing to understanding the essential functions of mitochondria, defined in the broadest sense, and the limits to which reductive evolution can proceed while maintaining a viable organelle.
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Leger, Michelle M., Markéta Petrů, Vojtěch Žárský, Laura Eme, Čestmír Vlček, Tommy Harding, B. Franz Lang, Marek Eliáš, Pavel Doležal i Andrew J. Roger. "An ancestral bacterial division system is widespread in eukaryotic mitochondria". Proceedings of the National Academy of Sciences 112, nr 33 (23.03.2015): 10239–46. http://dx.doi.org/10.1073/pnas.1421392112.
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Bacterial division initiates at the site of a contractile Z-ring composed of polymerized FtsZ. The location of the Z-ring in the cell is controlled by a system of three mutually antagonistic proteins, MinC, MinD, and MinE. Plastid division is also known to be dependent on homologs of these proteins, derived from the ancestral cyanobacterial endosymbiont that gave rise to plastids. In contrast, the mitochondria of model systems such asSaccharomyces cerevisiae, mammals, andArabidopsis thalianaseem to have replaced the ancestral α-proteobacterial Min-based division machinery with host-derived dynamin-related proteins that form outer contractile rings. Here, we show that the mitochondrial division system of these model organisms is the exception, rather than the rule, for eukaryotes. We describe endosymbiont-derived, bacterial-like division systems comprising FtsZ and Min proteins in diverse less-studied eukaryote protistan lineages, including jakobid and heterolobosean excavates, a malawimonad, stramenopiles, amoebozoans, a breviate, and an apusomonad. For two of these taxa, the amoebozoanDictyostelium purpureumand the jakobidAndalucia incarcerata, we confirm a mitochondrial localization of these proteins by their heterologous expression inSaccharomyces cerevisiae. The discovery of a proteobacterial-like division system in mitochondria of diverse eukaryotic lineages suggests that it was the ancestral feature of all eukaryotic mitochondria and has been supplanted by a host-derived system multiple times in distinct eukaryote lineages.
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Karnkowska, Anna, Sebastian C. Treitli, Ondřej Brzoň, Lukáš Novák, Vojtěch Vacek, Petr Soukal, Lael D. Barlow i in. "The Oxymonad Genome Displays Canonical Eukaryotic Complexity in the Absence of a Mitochondrion". Molecular Biology and Evolution 36, nr 10 (6.08.2019): 2292–312. http://dx.doi.org/10.1093/molbev/msz147.
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AbstractThe discovery that the protist Monocercomonoides exilis completely lacks mitochondria demonstrates that these organelles are not absolutely essential to eukaryotic cells. However, the degree to which the metabolism and cellular systems of this organism have adapted to the loss of mitochondria is unknown. Here, we report an extensive analysis of the M. exilis genome to address this question. Unexpectedly, we find that M. exilis genome structure and content is similar in complexity to other eukaryotes and less “reduced” than genomes of some other protists from the Metamonada group to which it belongs. Furthermore, the predicted cytoskeletal systems, the organization of endomembrane systems, and biosynthetic pathways also display canonical eukaryotic complexity. The only apparent preadaptation that permitted the loss of mitochondria was the acquisition of the SUF system for Fe–S cluster assembly and the loss of glycine cleavage system. Changes in other systems, including in amino acid metabolism and oxidative stress response, were coincident with the loss of mitochondria but are likely adaptations to the microaerophilic and endobiotic niche rather than the mitochondrial loss per se. Apart from the lack of mitochondria and peroxisomes, we show that M. exilis is a fully elaborated eukaryotic cell that is a promising model system in which eukaryotic cell biology can be investigated in the absence of mitochondria.
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Embley, Martin, Mark van der Giezen, David S. Horner, Patricia L. Dyal i Peter Foster. "Mitochondria and hydrogenosomes are two forms of the same fundamental organelle". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, nr 1429 (29.01.2003): 191–203. http://dx.doi.org/10.1098/rstb.2002.1190.
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Published data suggest that hydrogenosomes, organelles found in diverse anaerobic eukaryotes that make energy and hydrogen, were once mitochondria. As hydrogenosomes generally lack a genome, the conversion is probably one way. The sources of the key hydrogenosomal enzymes, pyruvate : ferredoxin oxidoreductase (PFO) and hydrogenase, are not resolved by current phylogenetic analyses, but it is likely that both were present at an early stage of eukaryotic evolution. Once thought to be restricted to a few unusual anaerobic eukaryotes, the proteins are intimately integrated into the fabric of diverse eukaryotic cells, where they are targeted to different cell compartments, and not just hydrogenosomes. There is no evidence supporting the view that PFO and hydrogenase originated from the mitochondrial endosymbiont, as posited by the hydrogen hypothesis for eukaryogenesis. Other organelles derived from mitochondria have now been described in anaerobic and parasitic microbial eukaryotes, including species that were once thought to have diverged before the mitochondrial symbiosis. It thus seems possible that all eukaryotes may eventually be shown to contain an organelle of mitochondrial ancestry, to which different types of biochemistry can be targeted. It remains to be seen if, despite their obvious differences, this family of organelles shares a common function of importance for the eukaryotic cell, other than energy production, that might provide the underlying selection pressure for organelle retention.
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Mills, Daniel B. "The origin of phagocytosis in Earth history". Interface Focus 10, nr 4 (12.06.2020): 20200019. http://dx.doi.org/10.1098/rsfs.2020.0019.
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Phagocytosis, or ‘cell eating’, is a eukaryote-specific process where particulate matter is engulfed via invaginations of the plasma membrane. The origin of phagocytosis has been central to discussions on eukaryogenesis for decades, where it is argued as being either a prerequisite for, or consequence of, the acquisition of the ancestral mitochondrion. Recently, genomic and cytological evidence has increasingly supported the view that the pre-mitochondrial host cell—a bona fide archaeon branching within the ‘Asgard’ archaea—was incapable of phagocytosis and used alternative mechanisms to incorporate the alphaproteobacterial ancestor of mitochondria. Indeed, the diversity and variability of proteins associated with phagosomes across the eukaryotic tree suggest that phagocytosis, as seen in a variety of extant eukaryotes, may have evolved independently several times within the eukaryotic crown-group. Since phagocytosis is critical to the functioning of modern marine food webs (without it, there would be no microbial loop or animal life), multiple late origins of phagocytosis could help explain why many of the ecological and evolutionary innovations of the Neoproterozoic Era (e.g. the advent of eukaryotic biomineralization, the ‘Rise of Algae’ and the origin of animals) happened when they did.
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Andersson, G. E., Olof Karlberg, Björn Canbäck i Charles G. Kurland. "On the origin of mitochondria: a genomics perspective". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, nr 1429 (29.01.2003): 165–79. http://dx.doi.org/10.1098/rstb.2002.1193.
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The availability of complete genome sequence data from both bacteria and eukaryotes provides information about the contribution of bacterial genes to the origin and evolution of mitochondria. Phylogenetic analyses based on genes located in the mitochondrial genome indicate that these genes originated from within the α–proteobacteria. A number of ancestral bacterial genes have also been transferred from the mitochondrial to the nuclear genome, as evidenced by the presence of orthologous genes in the mitochondrial genome in some species and in the nuclear genome of other species. However, a multitude of mitochondrial proteins encoded in the nucleus display no homology to bacterial proteins, indicating that these originated within the eukaryotic cell subsequent to the acquisition of the endosymbiont. An analysis of the expression patterns of yeast nuclear genes coding for mitochondrial proteins has shown that genes predicted to be of eukaryotic origin are mainly translated on polysomes that are free in the cytosol whereas those of putative bacterial origin are translated on polysomes attached to the mitochondrion. The strong relationship with α–proteobacterial genes observed for some mitochondrial genes, combined with the lack of such a relationship for others, indicates that the modern mitochondrial proteome is the product of both reductive and expansive processes.
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Eriso⃰, Feleke. "Human Genome & Origin of Mitochondria". European Journal of Biology and Medical Science Research 10, nr 4 (15.04.2022): 33–56. http://dx.doi.org/10.37745/ejbmsr.2013/vol10n43356.
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It had been believed that when individual eukaryotic cells engulfed aerobic and photosynthetic bacteria, the bacteria became endosymbionts with the phagocyte and evolved into mitochondria and chloroplasts respectively. The key objective of this study is to prove that the Endosymbiotic Theqory about the origins of mitochondria and chloroplasts is a misleading lie, being ridiculously laughable. Each of the micrographs or videos in the Figures, and each of the concrete evidences listed were designed to have targetful aims. The micrographs, videos, and concrete evidences were devised to serve as addressive findings (results). The human mitochondrial DNA is a transcript obtained when two separate spliced or mature RNAs (of DNA type) transcribed from the nuclear Genome of human oocyte have annealed into double-stranded transcript and exported into the cytoplasmic organelle called mitochondrion (plural, mitochondria) that mainly performs the task of producing energy (ATP) to power the genomic reactions of the cell. Lynn Margulis’s Endosymbiotic Theory which stated that mitochondrion & chloroplast found in eukaryotic cells had evolved from bacteria when they were engulfed by eukaryotic cells, was a misleading lie that would had been ridiculously laughable!!!!
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Björkholm, Patrik, Ajith Harish, Erik Hagström, Andreas M. Ernst i Siv G. E. Andersson. "Mitochondrial genomes are retained by selective constraints on protein targeting". Proceedings of the National Academy of Sciences 112, nr 33 (20.07.2015): 10154–61. http://dx.doi.org/10.1073/pnas.1421372112.
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Mitochondria are energy-producing organelles in eukaryotic cells considered to be of bacterial origin. The mitochondrial genome has evolved under selection for minimization of gene content, yet it is not known why not all mitochondrial genes have been transferred to the nuclear genome. Here, we predict that hydrophobic membrane proteins encoded by the mitochondrial genomes would be recognized by the signal recognition particle and targeted to the endoplasmic reticulum if they were nuclear-encoded and translated in the cytoplasm. Expression of the mitochondrially encoded proteins Cytochrome oxidase subunit 1, Apocytochrome b, and ATP synthase subunit 6 in the cytoplasm of HeLa cells confirms export to the endoplasmic reticulum. To examine the extent to which the mitochondrial proteome is driven by selective constraints within the eukaryotic cell, we investigated the occurrence of mitochondrial protein domains in bacteria and eukaryotes. The accessory protein domains of the oxidative phosphorylation system are unique to mitochondria, indicating the evolution of new protein folds. Most of the identified domains in the accessory proteins of the ribosome are also found in eukaryotic proteins of other functions and locations. Overall, one-third of the protein domains identified in mitochondrial proteins are only rarely found in bacteria. We conclude that the mitochondrial genome has been maintained to ensure the correct localization of highly hydrophobic membrane proteins. Taken together, the results suggest that selective constraints on the eukaryotic cell have played a major role in modulating the evolution of the mitochondrial genome and proteome.
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Emelyanov, Victor V. "Rickettsiaceae, Rickettsia-Like Endosymbionts, and the Origin of Mitochondria". Bioscience Reports 21, nr 1 (1.02.2001): 1–17. http://dx.doi.org/10.1023/a:1010409415723.
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Accumulating evolutionary data point to a monophyletic origin of mitochondria from the order Rickettsiales. This large group of obligate intracellular α-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.
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ChrzanowskaLightowlers, Zofia M. "Mitochondrial RNA and its eccentricities". Biochemist 37, nr 2 (1.04.2015): 28–32. http://dx.doi.org/10.1042/bio03702028.
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For those who do not work on mitochondria, their knowledge is often restricted to eubacterial origins, production of ATP and perhaps an appreciation of the non-Mendelian maternal inheritance patterns. These features are true enough, but things then start to get more complicated. Although the origins of mitochondria are accepted as a eubacterial endosymbiont of evolving eukaryotic cells1, there were organisms that were described as having jettisoned these ‘organelles’, referred to as amitochondriate eukaryotes. This concept has been challenged, and rudimentary mitochondria, or mitosomes, have now been found in those eukaryotes, which are apparently reluctant to lose this organelle2. The consequences of mitochondrial evolution can be seen in the divergence from the standard repertoire of RNA elements. These eccentricities pose challenges to our understanding of molecular mechanisms underlying mitochondrial gene expression.
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Dyall, Sabrina D., Carla M. Koehler, Maria G. Delgadillo-Correa, Peter J. Bradley, Evelyn Plümper, Danielle Leuenberger, Christoph W. Turck i Patricia J. Johnson. "Presence of a Member of the Mitochondrial Carrier Family in Hydrogenosomes: Conservation of Membrane-Targeting Pathways between Hydrogenosomes and Mitochondria". Molecular and Cellular Biology 20, nr 7 (1.04.2000): 2488–97. http://dx.doi.org/10.1128/mcb.20.7.2488-2497.2000.
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ABSTRACT A number of microaerophilic eukaryotes lack mitochondria but possess another organelle involved in energy metabolism, the hydrogenosome. Limited phylogenetic analyses of nuclear genes support a common origin for these two organelles. We have identified a protein of the mitochondrial carrier family in the hydrogenosome ofTrichomonas vaginalis and have shown that this protein, Hmp31, is phylogenetically related to the mitochondrial ADP-ATP carrier (AAC). We demonstrate that the hydrogenosomal AAC can be targeted to the inner membrane of mitochondria isolated from Saccharomyces cerevisiae through the Tim9-Tim10 import pathway used for the assembly of mitochondrial carrier proteins. Conversely, yeast mitochondrial AAC can be targeted into the membranes of hydrogenosomes. The hydrogenosomal AAC contains a cleavable, N-terminal presequence; however, this sequence is not necessary for targeting the protein to the organelle. These data indicate that the membrane-targeting signal(s) for hydrogenosomal AAC is internal, similar to that found for mitochondrial carrier proteins. Our findings indicate that the membrane carriers and membrane protein-targeting machinery of hydrogenosomes and mitochondria have a common evolutionary origin. Together, they provide strong evidence that a single endosymbiont evolved into a progenitor organelle in early eukaryotic cells that ultimately give rise to these two distinct organelles and support the hydrogen hypothesis for the origin of the eukaryotic cell.
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Lithgow, Trevor, i André Schneider. "Evolution of macromolecular import pathways in mitochondria, hydrogenosomes and mitosomes". Philosophical Transactions of the Royal Society B: Biological Sciences 365, nr 1541 (12.03.2010): 799–817. http://dx.doi.org/10.1098/rstb.2009.0167.
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All eukaryotes require mitochondria for survival and growth. The origin of mitochondria can be traced down to a single endosymbiotic event between two probably prokaryotic organisms. Subsequent evolution has left mitochondria a collection of heterogeneous organelle variants. Most of these variants have retained their own genome and translation system. In hydrogenosomes and mitosomes, however, the entire genome was lost. All types of mitochondria import most of their proteome from the cytosol, irrespective of whether they have a genome or not. Moreover, in most eukaryotes, a variable number of tRNAs that are required for mitochondrial translation are also imported. Thus, import of macromolecules, both proteins and tRNA, is essential for mitochondrial biogenesis. Here, we review what is known about the evolutionary history of the two processes using a recently revised eukaryotic phylogeny as a framework. We discuss how the processes of protein import and tRNA import relate to each other in an evolutionary context.
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Mentel, Marek, i William Martin. "Energy metabolism among eukaryotic anaerobes in light of Proterozoic ocean chemistry". Philosophical Transactions of the Royal Society B: Biological Sciences 363, nr 1504 (9.05.2008): 2717–29. http://dx.doi.org/10.1098/rstb.2008.0031.
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Recent years have witnessed major upheavals in views about early eukaryotic evolution. One very significant finding was that mitochondria, including hydrogenosomes and the newly discovered mitosomes, are just as ubiquitous and defining among eukaryotes as the nucleus itself. A second important advance concerns the readjustment, still in progress, about phylogenetic relationships among eukaryotic groups and the roughly six new eukaryotic supergroups that are currently at the focus of much attention. From the standpoint of energy metabolism (the biochemical means through which eukaryotes gain their ATP, thereby enabling any and all evolution of other traits), understanding of mitochondria among eukaryotic anaerobes has improved. The mainstream formulations of endosymbiotic theory did not predict the ubiquity of mitochondria among anaerobic eukaryotes, while an alternative hypothesis that specifically addressed the evolutionary origin of energy metabolism among eukaryotic anaerobes did. Those developments in biology have been paralleled by a similar upheaval in the Earth sciences regarding views about the prevalence of oxygen in the oceans during the Proterozoic (the time from ca 2.5 to 0.6 Ga ago). The new model of Proterozoic ocean chemistry indicates that the oceans were anoxic and sulphidic during most of the Proterozoic. Its proponents suggest the underlying geochemical mechanism to entail the weathering of continental sulphides by atmospheric oxygen to sulphate, which was carried into the oceans as sulphate, fuelling marine sulphate reducers (anaerobic, hydrogen sulphide-producing prokaryotes) on a global scale. Taken together, these two mutually compatible developments in biology and geology underscore the evolutionary significance of oxygen-independent ATP-generating pathways in mitochondria, including those of various metazoan groups, as a watermark of the environments within which eukaryotes arose and diversified into their major lineages.
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Speijer, Dave. "Being right on Q: shaping eukaryotic evolution". Biochemical Journal 473, nr 22 (10.11.2016): 4103–27. http://dx.doi.org/10.1042/bcj20160647.
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Reactive oxygen species (ROS) formation by mitochondria is an incompletely understood eukaryotic process. I proposed a kinetic model [BioEssays (2011) 33, 88–94] in which the ratio between electrons entering the respiratory chain via FADH2 or NADH (the F/N ratio) is a crucial determinant of ROS formation. During glucose breakdown, the ratio is low, while during fatty acid breakdown, the ratio is high (the longer the fatty acid, the higher is the ratio), leading to higher ROS levels. Thus, breakdown of (very-long-chain) fatty acids should occur without generating extra FADH2 in mitochondria. This explains peroxisome evolution. A potential ROS increase could also explain the absence of fatty acid oxidation in long-lived cells (neurons) as well as other eukaryotic adaptations, such as dynamic supercomplex formation. Effective combinations of metabolic pathways from the host and the endosymbiont (mitochondrion) allowed larger varieties of substrates (with different F/N ratios) to be oxidized, but high F/N ratios increase ROS formation. This might have led to carnitine shuttles, uncoupling proteins, and multiple antioxidant mechanisms, especially linked to fatty acid oxidation [BioEssays (2014) 36, 634–643]. Recent data regarding peroxisome evolution and their relationships with mitochondria, ROS formation by Complex I during ischaemia/reperfusion injury, and supercomplex formation adjustment to F/N ratios strongly support the model. I will further discuss the model in the light of experimental findings regarding mitochondrial ROS formation.
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Lane, Nick. "Origin of the Eukaryotic Cell". Molecular Frontiers Journal 01, nr 02 (grudzień 2017): 108–20. http://dx.doi.org/10.1142/s2529732517400120.
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All complex life on Earth is composed of ‘eukaryotic’ cells. Eukaryotes arose just once in 4 billion years, via an endosymbiosis — bacteria entered a simple host cell, evolving into mitochondria, the ‘powerhouses’ of complex cells. Mitochondria lost most of their genes, retaining only those needed for respiration, giving eukaryotes ‘multi-bacterial’ power without the costs of maintaining thousands of complete bacterial genomes. These energy savings supported a substantial expansion in nuclear genome size, and far more protein synthesis from each gene.
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Van der Giezen, Mark. "Eukaryotic life without mitochondria?" Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 153, nr 2 (czerwiec 2009): S165—S166. http://dx.doi.org/10.1016/j.cbpa.2009.04.339.
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Graf, Jon S., Sina Schorn, Katharina Kitzinger, Soeren Ahmerkamp, Christian Woehle, Bruno Huettel, Carsten J. Schubert, Marcel M. M. Kuypers i Jana Milucka. "Anaerobic endosymbiont generates energy for ciliate host by denitrification". Nature 591, nr 7850 (3.03.2021): 445–50. http://dx.doi.org/10.1038/s41586-021-03297-6.
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AbstractMitochondria are specialized eukaryotic organelles that have a dedicated function in oxygen respiration and energy production. They evolved about 2 billion years ago from a free-living bacterial ancestor (probably an alphaproteobacterium), in a process known as endosymbiosis1,2. Many unicellular eukaryotes have since adapted to life in anoxic habitats and their mitochondria have undergone further reductive evolution3. As a result, obligate anaerobic eukaryotes with mitochondrial remnants derive their energy mostly from fermentation4. Here we describe ‘Candidatus Azoamicus ciliaticola’, which is an obligate endosymbiont of an anaerobic ciliate and has a dedicated role in respiration and providing energy for its eukaryotic host. ‘Candidatus A. ciliaticola’ contains a highly reduced 0.29-Mb genome that encodes core genes for central information processing, the electron transport chain, a truncated tricarboxylic acid cycle, ATP generation and iron–sulfur cluster biosynthesis. The genome encodes a respiratory denitrification pathway instead of aerobic terminal oxidases, which enables its host to breathe nitrate instead of oxygen. ‘Candidatus A. ciliaticola’ and its ciliate host represent an example of a symbiosis that is based on the transfer of energy in the form of ATP, rather than nutrition. This discovery raises the possibility that eukaryotes with mitochondrial remnants may secondarily acquire energy-providing endosymbionts to complement or replace functions of their mitochondria.
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Włoga, D., I. Strzyżewska-Jówko, J. Gaertig i M. Jerka-Dziadosz. "Septins Stabilize Mitochondria in Tetrahymena thermophila". Eukaryotic Cell 7, nr 8 (27.06.2008): 1373–86. http://dx.doi.org/10.1128/ec.00085-08.
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ABSTRACT We describe phylogenetic and functional studies of three septins in the free-living ciliate Tetrahymena thermophila. Both deletion and overproduction of septins led to vacuolization of mitochondria, destabilization of the nuclear envelope, and increased autophagy. All three green fluorescent protein-tagged septins localized to mitochondria. Specific septins localized to the outer mitochondrial membrane, to septa formed during mitochondrial scission, or to the mitochondrion-associated endoplasmic reticulum. The only other septins known to localize to mitochondria are human ARTS and murine M-septin, both alternatively spliced forms of Sep4 (S. Larisch, Cell Cycle 3:1021-1023, 2004; S. Takahashi, R. Inatome, H. Yamamura, and S. Yanagi, Genes Cells 8:81-93, 2003). It therefore appears that septins have been recruited to mitochondrial functions independently in at least two eukaryotic lineages and in both cases are involved in apoptotic events.
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Ku, Chuan, Shijulal Nelson-Sathi, Mayo Roettger, Sriram Garg, Einat Hazkani-Covo i William F. Martin. "Endosymbiotic gene transfer from prokaryotic pangenomes: Inherited chimerism in eukaryotes". Proceedings of the National Academy of Sciences 112, nr 33 (2.03.2015): 10139–46. http://dx.doi.org/10.1073/pnas.1421385112.
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Endosymbiotic theory in eukaryotic-cell evolution rests upon a foundation of three cornerstone partners—the plastid (a cyanobacterium), the mitochondrion (a proteobacterium), and its host (an archaeon)—and carries a corollary that, over time, the majority of genes once present in the organelle genomes were relinquished to the chromosomes of the host (endosymbiotic gene transfer). However, notwithstanding eukaryote-specific gene inventions, single-gene phylogenies have never traced eukaryotic genes to three single prokaryotic sources, an issue that hinges crucially upon factors influencing phylogenetic inference. In the age of genomes, single-gene trees, once used to test the predictions of endosymbiotic theory, now spawn new theories that stand to eventually replace endosymbiotic theory with descriptive, gene tree-based variants featuring supernumerary symbionts: prokaryotic partners distinct from the cornerstone trio and whose existence is inferred solely from single-gene trees. We reason that the endosymbiotic ancestors of mitochondria and chloroplasts brought into the eukaryotic—and plant and algal—lineage a genome-sized sample of genes from the proteobacterial and cyanobacterial pangenomes of their respective day and that, even if molecular phylogeny were artifact-free, sampling prokaryotic pangenomes through endosymbiotic gene transfer would lead to inherited chimerism. Recombination in prokaryotes (transduction, conjugation, transformation) differs from recombination in eukaryotes (sex). Prokaryotic recombination leads to pangenomes, and eukaryotic recombination leads to vertical inheritance. Viewed from the perspective of endosymbiotic theory, the critical transition at the eukaryote origin that allowed escape from Muller’s ratchet—the origin of eukaryotic recombination, or sex—might have required surprisingly little evolutionary innovation.
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Lu, Peiran, Siau Yen Wong, Lei Wu i Dingbo Lin. "Carotenoid metabolism in mitochondrial function". Food Quality and Safety 4, nr 3 (sierpień 2020): 115–22. http://dx.doi.org/10.1093/fqsafe/fyaa023.
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Abstract Mitochondria are highly dynamic organelles that are found in most eukaryotic organisms. It is broadly accepted that mitochondria originally evolved from prokaryotic bacteria, e.g. proteobacteria. The mitochondrion has its independent genome that encodes 37 genes, including 13 genes for oxidative phosphorylation. Accumulative evidence demonstrates that mitochondria are not only the powerhouse of the cells by supplying adenosine triphosphate, but also exert roles as signalling organelles in the cell fate and function. Numerous factors can affect mitochondria structurally and functionally. Carotenoids are a large group of fat-soluble pigments commonly found in our diets. Recently, much attention has been paid in carotenoids as dietary bioactives in mitochondrial structure and function in human health and disease, though the mechanistic research is limited. Here, we update the recent progress in mitochondrial functioning as signalling organelles in human health and disease, summarize the potential roles of carotenoids in regulation of mitochondrial redox homeostasis, biogenesis, and mitophagy, and discuss the possible approaches for future research in carotenoid regulation of mitochondrial function.
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Barnhill, Alison E., Matt T. Brewer i Steve A. Carlson. "Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components". Antimicrobial Agents and Chemotherapy 56, nr 8 (21.05.2012): 4046–51. http://dx.doi.org/10.1128/aac.00678-12.
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ABSTRACTThis minireview explores mitochondria as a site for antibiotic-host interactions that lead to pathophysiologic responses manifested as nonantibacterial side effects. Mitochondrion-based side effects are possibly related to the notion that these organelles are archaic bacterial ancestors or commandeered remnants that have co-evolved in eukaryotic cells; thus, this minireview focuses on mitochondrial damage that may be analogous to the antibacterial effects of the drugs. Special attention is devoted to aminoglycosides, chloramphenicol, and fluoroquinolones and their respective single side effects related to mitochondrial disturbances. Linezolid/oxazolidinone multisystemic toxicity is also discussed. Aminoglycosides and oxazolidinones are inhibitors of bacterial ribosomes, and some of their side effects appear to be based on direct inhibition of mitochondrial ribosomes. Chloramphenicol and fluoroquinolones target bacterial ribosomes and gyrases/topoisomerases, respectively, both of which are present in mitochondria. However, the side effects of chloramphenicol and the fluoroquinolones appear to be based on idiosyncratic damage to host mitochondria. Nonetheless, it appears that mitochondrion-associated side effects are a potential aspect of antibiotics whose targets are shared by prokaryotes and mitochondria—an important consideration for future drug design.
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Medini, Hadar, Tal Cohen i Dan Mishmar. "Mitochondria Are Fundamental for the Emergence of Metazoans: On Metabolism, Genomic Regulation, and the Birth of Complex Organisms". Annual Review of Genetics 54, nr 1 (23.11.2020): 151–66. http://dx.doi.org/10.1146/annurev-genet-021920-105545.
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Out of many intracellular bacteria, only the mitochondria and chloroplasts abandoned their independence billions of years ago and became endosymbionts within the host eukaryotic cell. Consequently, one cannot grow eukaryotic cells without their mitochondria, and the mitochondria cannot divide outside of the cell, thus reflecting interdependence. Here, we argue that such interdependence underlies the fundamental role of mitochondrial activities in the emergence of metazoans. Several lines of evidence support our hypothesis: ( a) Differentiation and embryogenesis rely on mitochondrial function; ( b) mitochondrial metabolites are primary precursors for epigenetic modifications (such as methyl and acetyl), which are critical for chromatin remodeling and gene expression, particularly during differentiation and embryogenesis; and ( c) mitonuclear coregulation adapted to accommodate both housekeeping and tissue-dependent metabolic needs. We discuss the evolution of the unique mitochondrial genetic system, mitochondrial metabolites, mitonuclear coregulation, and their critical roles in the emergence of metazoans and in human disorders.
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Oborník, Miroslav. "Enigmatic Evolutionary History of Porphobilinogen Deaminase in Eukaryotic Phototrophs". Biology 10, nr 5 (29.04.2021): 386. http://dx.doi.org/10.3390/biology10050386.
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In most eukaryotic phototrophs, the entire heme synthesis is localized to the plastid, and enzymes of cyanobacterial origin dominate the pathway. Despite that, porphobilinogen deaminase (PBGD), the enzyme responsible for the synthesis of hydroxymethybilane in the plastid, shows phylogenetic affiliation to α-proteobacteria, the supposed ancestor of mitochondria. Surprisingly, no PBGD of such origin is found in the heme pathway of the supposed partners of the primary plastid endosymbiosis, a primarily heterotrophic eukaryote, and a cyanobacterium. It appears that α-proteobacterial PBGD is absent from glaucophytes but is present in rhodophytes, chlorophytes, plants, and most algae with complex plastids. This may suggest that in eukaryotic phototrophs, except for glaucophytes, either the gene from the mitochondrial ancestor was retained while the cyanobacterial and eukaryotic pseudoparalogs were lost in evolution, or the gene was acquired by non-endosymbiotic gene transfer from an unspecified α-proteobacterium and functionally replaced its cyanobacterial and eukaryotic counterparts.
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Luna-Sánchez, Marta, Patrizia Bianchi i Albert Quintana. "Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within". International Journal of Molecular Sciences 22, nr 16 (7.08.2021): 8523. http://dx.doi.org/10.3390/ijms22168523.
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Symbiosis between the mitochondrion and the ancestor of the eukaryotic cell allowed cellular complexity and supported life. Mitochondria have specialized in many key functions ensuring cell homeostasis and survival. Thus, proper communication between mitochondria and cell nucleus is paramount for cellular health. However, due to their archaebacterial origin, mitochondria possess a high immunogenic potential. Indeed, mitochondria have been identified as an intracellular source of molecules that can elicit cellular responses to pathogens. Compromised mitochondrial integrity leads to release of mitochondrial content into the cytosol, which triggers an unwanted cellular immune response. Mitochondrial nucleic acids (mtDNA and mtRNA) can interact with the same cytoplasmic sensors that are specialized in recognizing genetic material from pathogens. High-energy demanding cells, such as neurons, are highly affected by deficits in mitochondrial function. Notably, mitochondrial dysfunction, neurodegeneration, and chronic inflammation are concurrent events in many severe debilitating disorders. Interestingly in this context of pathology, increasing number of studies have detected immune-activating mtDNA and mtRNA that induce an aberrant production of pro-inflammatory cytokines and interferon effectors. Thus, this review provides new insights on mitochondria-driven inflammation as a potential therapeutic target for neurodegenerative and primary mitochondrial diseases.
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Knorre, Dmitry A., Konstantin Y. Popadin, Svyatoslav S. Sokolov i Fedor F. Severin. "Roles of Mitochondrial Dynamics under Stressful and Normal Conditions in Yeast Cells". Oxidative Medicine and Cellular Longevity 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/139491.
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Eukaryotic cells contain dynamic mitochondrial filaments: they fuse and divide. Here we summarize data on the protein machinery driving mitochondrial dynamics in yeast and also discuss the factors that affect the fusion-fission balance. Fission is a general stress response of cells, and in the case of yeast this response appears to be prosurvival. At the same time, even under normal conditions yeast mitochondria undergo continuous cycles of fusion and fission. This seems to be a futile cycle and also expensive from the energy point of view. Why does it exist? Benefits might be the same as in the case of sexual reproduction. Indeed, mixing and separating of mitochondrial content allows mitochondrial DNA to segregate and recombine randomly, leading to high variation in the numbers of mutations per individual mitochondrion. This opens a possibility for effective purifying selection-elimination of mitochondria highly contaminated by deleterious mutations. The beneficial action presumes a mechanism for removal of defective mitochondria. We argue that selective mitochondrial autophagy or asymmetrical distribution of mitochondria during cell division could be at the core of such mechanism.
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Jeena, M. T., Sangpil Kim, Seongeon Jin i Ja-Hyoung Ryu. "Recent Progress in Mitochondria-Targeted Drug and Drug-Free Agents for Cancer Therapy". Cancers 12, nr 1 (18.12.2019): 4. http://dx.doi.org/10.3390/cancers12010004.
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The mitochondrion is a dynamic eukaryotic organelle that controls lethal and vital functions of the cell. Being a critical center of metabolic activities and involved in many diseases, mitochondria have been attracting attention as a potential target for therapeutics, especially for cancer treatment. Structural and functional differences between healthy and cancerous mitochondria, such as membrane potential, respiratory rate, energy production pathway, and gene mutations, could be employed for the design of selective targeting systems for cancer mitochondria. A number of mitochondria-targeting compounds, including mitochondria-directed conventional drugs, mitochondrial proteins/metabolism-inhibiting agents, and mitochondria-targeted photosensitizers, have been discussed. Recently, certain drug-free approaches have been introduced as an alternative to induce selective cancer mitochondria dysfunction, such as intramitochondrial aggregation, self-assembly, and biomineralization. In this review, we discuss the recent progress in mitochondria-targeted cancer therapy from the conventional approach of drug/cytotoxic agent conjugates to advanced drug-free approaches.
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Hackstein, J. H. P. "Eukaryotic Fe-hydrogenases – old eukaryotic heritage or adaptive acquisitions?" Biochemical Society Transactions 33, nr 1 (1.02.2005): 47–50. http://dx.doi.org/10.1042/bst0330047.
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All eukaryotes seem to possess proteins that most probably evolved from an ancestral Fe-hydrogenase. These proteins, known as NARF or Nar, do not produce hydrogen. Notably, a small group of rather unrelated unicellular anaerobes and a few algae possess Fe-hydrogenases, which produce hydrogen. In most, but not all organisms, hydrogen production occurs in membrane-bounded organelles, i.e. hydrogenosomes or plastids. Whereas plastids are monophyletic, hydrogenosomes evolved repeatedly and independently from mitochondria or mitochondria-like organelles. A systematic analysis of the various hydrogenosomes and their hydrogenases will contribute to an understanding of the evolution of the eukaryotic cell, and provide clues to the evolutionary origin(s) of the Fe-hydrogenase.
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Anselmetti, Yoann, Nadia El-Mabrouk, Manuel Lafond i Aïda Ouangraoua. "Gene tree and species tree reconciliation with endosymbiotic gene transfer". Bioinformatics 37, Supplement_1 (1.07.2021): i120—i132. http://dx.doi.org/10.1093/bioinformatics/btab328.
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Abstract Motivation It is largely established that all extant mitochondria originated from a unique endosymbiotic event integrating an α−proteobacterial genome into an eukaryotic cell. Subsequently, eukaryote evolution has been marked by episodes of gene transfer, mainly from the mitochondria to the nucleus, resulting in a significant reduction of the mitochondrial genome, eventually completely disappearing in some lineages. However, in other lineages such as in land plants, a high variability in gene repertoire distribution, including genes encoded in both the nuclear and mitochondrial genome, is an indication of an ongoing process of Endosymbiotic Gene Transfer (EGT). Understanding how both nuclear and mitochondrial genomes have been shaped by gene loss, duplication and transfer is expected to shed light on a number of open questions regarding the evolution of eukaryotes, including rooting of the eukaryotic tree. Results We address the problem of inferring the evolution of a gene family through duplication, loss and EGT events, the latter considered as a special case of horizontal gene transfer occurring between the mitochondrial and nuclear genomes of the same species (in one direction or the other). We consider both EGT events resulting in maintaining (EGTcopy) or removing (EGTcut) the gene copy in the source genome. We present a linear-time algorithm for computing the DLE (Duplication, Loss and EGT) distance, as well as an optimal reconciled tree, for the unitary cost, and a dynamic programming algorithm allowing to output all optimal reconciliations for an arbitrary cost of operations. We illustrate the application of our EndoRex software and analyze different costs settings parameters on a plant dataset and discuss the resulting reconciled trees. Availability and implementation EndoRex implementation and supporting data are available on the GitHub repository via https://github.com/AEVO-lab/EndoRex.
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Fuchs, Florian, i Benedikt Westermann. "Role of Unc104/KIF1-related Motor Proteins in Mitochondrial Transport in Neurospora crassa". Molecular Biology of the Cell 16, nr 1 (styczeń 2005): 153–61. http://dx.doi.org/10.1091/mbc.e04-05-0413.
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Eukaryotic cells use diverse cytoskeleton-dependent machineries to control inheritance and intracellular positioning of mitochondria. In particular, microtubules play a major role in mitochondrial motility in the filamentous fungus Neurospora crassa and in mammalian cells. We examined the role of two novel Unc104/KIF1-related members of the kinesin family, Nkin2 and Nkin3, in mitochondrial motility in Neurospora. The Nkin2 protein is required for mitochondrial interactions with microtubules in vitro. Mutant hyphae lacking Nkin2 show mitochondrial motility defects in vivo early after germination of conidiospores. Nkin3, a member of a unique fungal-specific subgroup of small Unc104/KIF1-related proteins, is not associated with mitochondria in wild-type cells. However, it is highly expressed and recruited to mitochondria in Δnkin-2 mutants. Mitochondria lacking Nkin2 require Nkin3 for binding to microtubules in vitro, and mitochondrial motility defects in Δnkin-2 mutants disappear with up-regulation of Nkin3 in vivo. We propose that mitochondrial transport is mediated by Nkin2 in Neurospora, and organelle motility defects in Δnkin-2 mutants are rescued by Nkin3. Apparently, a highly versatile complement of organelle motors allows the cell to efficiently respond to exogenous challenges, a process that might also account for the great variety of different mitochondrial transport systems that have evolved in eukaryotic cells.
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Ayer, Anita, Ian W. Dawes i Gabriel G. Perrone. "Mitochondria, oxidative stress and the petite phenotype in Saccharomyces cerevisiae". Microbiology Australia 31, nr 2 (2010): 82. http://dx.doi.org/10.1071/ma10082.
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Oxidative stress has long been recognised as biologically important and is increasingly implicated in a variety of phenomena, such as mutation, carcinogenesis, degenerative and other diseases, inflammation, ageing, and development. The role of the mitochondrion in oxidative stress and the production of reactive oxygen species (ROS) and other radical species is well-established, with mitochondria providing a fascinating area of study within the oxidative stress field. Mitochondria are essential organelles for the viability of all eukaryotic organisms. While mitochondria perform important processes associated with oxidative phosphorylation and energy production, and numerous other metabolic processes, such as iron sulfur cluster biogenesis, lipid and amino acid synthesis, they also appear to be the largest intracellular source of ROS in aerobic cells. The steady state concentration of O2 in the mitochondrial matrix is five- to tenfold higher than in the cytosol or nuclear space according to one estimation. Therefore, mitochondrial macromolecules such as mitochondrial DNA are particularly susceptible to oxidative damage.
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da Cunha, Fernanda Marques, Nicole Quesada Torelli i Alicia J. Kowaltowski. "Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes". Oxidative Medicine and Cellular Longevity 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/482582.
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Mitochondria are essential organelles for eukaryotic homeostasis. Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus. This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus. Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.
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Charrière, Fabien, Patrick O'Donoghue, Sunna Helgadóttir, Laurence Maréchal-Drouard, Marina Cristodero, Elke K. Horn, Dieter Söll i André Schneider. "Dual Targeting of a tRNAAsp Requires Two Different Aspartyl-tRNA Synthetases in Trypanosoma brucei". Journal of Biological Chemistry 284, nr 24 (22.04.2009): 16210–17. http://dx.doi.org/10.1074/jbc.m109.005348.
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The mitochondrion of the parasitic protozoon Trypanosoma brucei does not encode any tRNAs. This deficiency is compensated for by partial import of nearly all of its cytosolic tRNAs. Most trypanosomal aminoacyl-tRNA synthetases are encoded by single copy genes, suggesting the use of the same enzyme in the cytosol and in the mitochondrion. However, the T. brucei genome encodes two distinct genes for eukaryotic aspartyl-tRNA synthetase (AspRS), although the cell has a single tRNAAsp isoacceptor only. Phylogenetic analysis showed that the two T. brucei AspRSs evolved from a duplication early in kinetoplastid evolution and also revealed that eight other major duplications of AspRS occurred in the eukaryotic domain. RNA interference analysis established that both Tb-AspRS1 and Tb-AspRS2 are essential for growth and required for cytosolic and mitochondrial Asp-tRNAAsp formation, respectively. In vitro charging assays demonstrated that the mitochondrial Tb-AspRS2 aminoacylates both cytosolic and mitochondrial tRNAAsp, whereas the cytosolic Tb-AspRS1 selectively recognizes cytosolic but not mitochondrial tRNAAsp. This indicates that cytosolic and mitochondrial tRNAAsp, although derived from the same nuclear gene, are physically different, most likely due to a mitochondria-specific nucleotide modification. Mitochondrial Tb-AspRS2 defines a novel group of eukaryotic AspRSs with an expanded substrate specificity that are restricted to trypanosomatids and therefore may be exploited as a novel drug target.
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Davuluri, Gangarao, Ping Song, Zhuoming Liu, David Wald, Takuya F. Sakaguchi, Michael R. Green i L. Devireddy. "Inactivation of 3-hydroxybutyrate dehydrogenase2 delays zebrafish erythroid maturation by conferring premature mitophagy". Proceedings of the National Academy of Sciences 113, nr 11 (29.02.2016): E1460—E1469. http://dx.doi.org/10.1073/pnas.1600077113.
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Mitochondria are the site of iron utilization, wherein imported iron is incorporated into heme or iron–sulfur clusters. Previously, we showed that a cytosolic siderophore, which resembles a bacterial siderophore, facilitates mitochondrial iron import in eukaryotes, including zebrafish. An evolutionarily conserved 3-hydroxy butyrate dehydrogenase, 3-hydroxy butyrate dehydrogenase 2 (Bdh2), catalyzes a rate-limiting step in the biogenesis of the eukaryotic siderophore. We found that inactivation ofbdh2 in developing zebrafish embryo results in heme deficiency and delays erythroid maturation. The basis for this erythroid maturation defect is not known. Here we show thatbdh2 inactivation results in mitochondrial dysfunction and triggers their degradation by mitophagy. Thus, mitochondria are prematurely lost inbdh2-inactivated erythrocytes. Interestingly,bdh2-inactivated erythroid cells also exhibit genomic alterations as indicated by transcriptome analysis. Reestablishment ofbdh2 restores mitochondrial function, prevents premature mitochondrial degradation, promotes erythroid development, and reverses altered gene expression. Thus, mitochondrial communication with the nucleus is critical for erythroid development.
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Bergstrom, Carl T., i Jonathan Pritchard. "Germline Bottlenecks and the Evolutionary Maintenance of Mitochondrial Genomes". Genetics 149, nr 4 (1.08.1998): 2135–46. http://dx.doi.org/10.1093/genetics/149.4.2135.
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Abstract Several features of the biology of mitochondria suggest that mitochondria might be susceptible to Muller's ratchet and other forms of evolutionary degradation: Mitochondria have predominantly uniparental inheritance, appear to be nonrecombining, and have high mutation rates producing significant deleterious variation. We demonstrate that the persistence of mitochondria may be explained by recent data that point to a severe “bottleneck” in the number of mitochondria passing through the germline in humans and other mammals. We present a population-genetic model in which deleterious mutations arise within individual mitochondria, while selection operates on assemblages of mitochondria at the level of their eukaryotic hosts. We show that a bottleneck increases the efficacy of selection against deleterious mutations by increasing the variance in fitness among eukaryotic hosts. We investigate both the equilibrium distribution of deleterious variation in large populations and the dynamics of Muller's ratchet in small populations. We find that in the absence of the ratchet, a bottleneck leads to improved mitochondrial performance and that, over a longer time scale, a bottleneck acts to slow the progression of the ratchet.
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Li, Xiaowen, Keke Wu, Sen Zeng, Feifan Zhao, Jindai Fan, Zhaoyao Li, Lin Yi i in. "Viral Infection Modulates Mitochondrial Function". International Journal of Molecular Sciences 22, nr 8 (20.04.2021): 4260. http://dx.doi.org/10.3390/ijms22084260.
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Mitochondria are important organelles involved in metabolism and programmed cell death in eukaryotic cells. In addition, mitochondria are also closely related to the innate immunity of host cells against viruses. The abnormality of mitochondrial morphology and function might lead to a variety of diseases. A large number of studies have found that a variety of viral infections could change mitochondrial dynamics, mediate mitochondria-induced cell death, and alter the mitochondrial metabolic status and cellular innate immune response to maintain intracellular survival. Meanwhile, mitochondria can also play an antiviral role during viral infection, thereby protecting the host. Therefore, mitochondria play an important role in the interaction between the host and the virus. Herein, we summarize how viral infections affect microbial pathogenesis by altering mitochondrial morphology and function and how viruses escape the host immune response.
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Ding, Di, Kunjan R. Dave i Sanjoy K. Bhattacharya. "On Message Ribonucleic Acids Targeting to Mitochondria". Biochemistry Insights 2 (styczeń 2009): BCI.S3745. http://dx.doi.org/10.4137/bci.s3745.
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Mitochondria are subcellular organelles that provide energy for a variety of basic cellular processes in eukaryotic cells. Mitochondria maintain their own genomes and many of their endosymbiont genes are encoded by nuclear genomes. The crosstalk between the mitochondrial and nuclear genomes ensures mitochondrial biogenesis, dynamics and maintenance. Mitochondrial proteins are partly encoded by nucleus and synthesized in the cytosol and partly in the mitochondria coded by mitochondrial genome. The efficiency of transport systems that transport nuclear encoded gene products such as proteins and mRNAs to the mitochondrial vicinity to allow for their translation and/or import are recently receiving wide attention. There is currently no concrete evidence that nuclear encoded mRNA is transported into the mitochondria, however, they can be transported onto the mitochondrial surface and translated at the surface of mitochondria utilizing cytosolic machinery. In this review we present an overview of the recent advances in the mRNA transport, with emphasis on the transport of nuclear-encoded mitochondrial protein mRNA into the mitochondria.
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Manzanares-Estreder, Sara, Amparo Pascual-Ahuir i Markus Proft. "Stress-Activated Degradation of Sphingolipids Regulates Mitochondrial Function and Cell Death in Yeast". Oxidative Medicine and Cellular Longevity 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/2708345.
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Sphingolipids are regulators of mitochondria-mediated cell death in higher eukaryotes. Here, we investigate how changes in sphingolipid metabolism and downstream intermediates of sphingosine impinge on mitochondrial function. We found in yeast that within the sphingolipid degradation pathway, the production via Dpl1p and degradation via Hfd1p of hexadecenal are critical for mitochondrial function and cell death. Genetic interventions, which favor hexadecenal accumulation, diminish oxygen consumption rates and increase reactive oxygen species production and mitochondrial fragmentation and vice versa. The location of the hexadecenal-degrading enzyme Hfd1p in punctuate structures all along the mitochondrial network depends on a functional ERMES (endoplasmic reticulum-mitochondria encounter structure) complex, indicating that modulation of hexadecenal levels at specific ER-mitochondria contact sites might be an important trigger of cell death. This is further supported by the finding that externally added hexadecenal or the absence of Hfd1p enhances cell death caused by ectopic expression of the human Bax protein. Finally, the induction of the sphingolipid degradation pathway upon stress is controlled by the Hog1p MAP kinase. Therefore, the stress-regulated modulation of sphingolipid degradation might be a conserved way to induce cell death in eukaryotic organisms.
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Schapira, Anthony. "Mitochondrial DNA and disease: What happens when things go wrong". Biochemist 27, nr 3 (1.06.2005): 24–27. http://dx.doi.org/10.1042/bio02703024.
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Mitochondria are ubiquitous in eukaryotic cells and one of their important functions is to provide ATP via oxidative phosphorylation (OXPHOS). The mitochondria also host other biochemical pathways, including -oxidation, Krebs' citric acid cycle and parts of the urea cycle. Thus, the mitochondria play a pivotal role in cellular biochemistry. The relationship of mitochondria to human disease has been identified only recently, but has now become one of the most rapidly expanding areas of human pathology. Mitochondrial disorders may be a consequence of inherited defects of either the nuclear or mitochondrial genomes or, alternatively, may be due to endogenous or exogenous environmental toxins. This article will focus upon abnormalities of mitochondrial DNA (mtDNA) and human disease.
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Breton, Sophie, i Donald T. Stewart. "Atypical mitochondrial inheritance patterns in eukaryotes". Genome 58, nr 10 (październik 2015): 423–31. http://dx.doi.org/10.1139/gen-2015-0090.
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Mitochondrial DNA (mtDNA) is predominantly maternally inherited in eukaryotes. Diverse molecular mechanisms underlying the phenomenon of strict maternal inheritance (SMI) of mtDNA have been described, but the evolutionary forces responsible for its predominance in eukaryotes remain to be elucidated. Exceptions to SMI have been reported in diverse eukaryotic taxa, leading to the prediction that several distinct molecular mechanisms controlling mtDNA transmission are present among the eukaryotes. We propose that these mechanisms will be better understood by studying the deviations from the predominating pattern of SMI. This minireview summarizes studies on eukaryote species with unusual or rare mitochondrial inheritance patterns, i.e., other than the predominant SMI pattern, such as maternal inheritance of stable heteroplasmy, paternal leakage of mtDNA, biparental and strictly paternal inheritance, and doubly uniparental inheritance of mtDNA. The potential genes and mechanisms involved in controlling mitochondrial inheritance in these organisms are discussed. The linkage between mitochondrial inheritance and sex determination is also discussed, given that the atypical systems of mtDNA inheritance examined in this minireview are frequently found in organisms with uncommon sexual systems such as gynodioecy, monoecy, or andromonoecy. The potential of deviations from SMI for facilitating a better understanding of a number of fundamental questions in biology, such as the evolution of mtDNA inheritance, the coevolution of nuclear and mitochondrial genomes, and, perhaps, the role of mitochondria in sex determination, is considerable.
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Hoshino, Yosuke, i Eric A. Gaucher. "Evolution of bacterial steroid biosynthesis and its impact on eukaryogenesis". Proceedings of the National Academy of Sciences 118, nr 25 (15.06.2021): e2101276118. http://dx.doi.org/10.1073/pnas.2101276118.
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Steroids are components of the eukaryotic cellular membrane and have indispensable roles in the process of eukaryotic endocytosis by regulating membrane fluidity and permeability. In particular, steroids may have been a structural prerequisite for the acquisition of mitochondria via endocytosis during eukaryogenesis. While eukaryotes are inferred to have evolved from an archaeal lineage, there is little similarity between the eukaryotic and archaeal cellular membranes. As such, the evolution of eukaryotic cellular membranes has limited our understanding of eukaryogenesis. Despite evolving from archaea, the eukaryotic cellular membrane is essentially a fatty acid bacterial-type membrane, which implies a substantial bacterial contribution to the evolution of the eukaryotic cellular membrane. Here, we address the evolution of steroid biosynthesis in eukaryotes by combining ancestral sequence reconstruction and comprehensive phylogenetic analyses of steroid biosynthesis genes. Contrary to the traditional assumption that eukaryotic steroid biosynthesis evolved within eukaryotes, most steroid biosynthesis genes are inferred to be derived from bacteria. In particular, aerobic deltaproteobacteria (myxobacteria) seem to have mediated the transfer of key genes for steroid biosynthesis to eukaryotes. Analyses of resurrected steroid biosynthesis enzymes suggest that the steroid biosynthesis pathway in early eukaryotes may have been similar to the pathway seen in modern plants and algae. These resurrected proteins also experimentally demonstrate that molecular oxygen was required to establish the modern eukaryotic cellular membrane during eukaryogenesis. Our study provides unique insight into relationships between early eukaryotes and other bacteria in addition to the well-known endosymbiosis with alphaproteobacteria.
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Jang, Yoon-ha, i Kwang-il Lim. "Recent Advances in Mitochondria-Targeted Gene Delivery". Molecules 23, nr 9 (11.09.2018): 2316. http://dx.doi.org/10.3390/molecules23092316.
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Mitochondria are the energy-producing organelles of cells. Mitochondrial dysfunctions link to various syndromes and diseases including myoclonic epilepsy and ragged-red fiber disease (MERRF), Leigh syndrome (LS), and Leber hereditary optic neuropathy (LHON). Primary mitochondrial diseases often result from mutations of mitochondrial genomes and nuclear genes that encode the mitochondrial components. However, complete intracellular correction of the mutated genetic parts relevant to mitochondrial structures and functions is technically challenging. Instead, there have been diverse attempts to provide corrected genetic materials with cells. In this review, we discuss recent novel physical, chemical and biological strategies, and methods to introduce genetic cargos into mitochondria of eukaryotic cells. Effective mitochondria-targeting gene delivery systems can reverse multiple mitochondrial disorders by enabling cells to produce functional mitochondrial components.
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Wang, Meng. "Microbiome-Mitochondria Communication in the Regulation of Host Longevity". Innovation in Aging 4, Supplement_1 (1.12.2020): 739. http://dx.doi.org/10.1093/geroni/igaa057.2637.
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Abstract Mitochondria are ancient relatives of bacteria in eukaryotic cells and dynamically interconnected through organelle fusion and fission. Given the close relationship between bacteria and eukaryotic mitochondria during evolution, my group is interested in understanding the critical role of their communication in regulating host’s longevity. We have conducted genome-scale screens to decipher how bacterial genetic composition impacts host longevity, leading to the discovery of specific bacteria-secreted metabolites that fine-tune the mitochondrial fusion-fission balance and consequently promotes longevity across different host species. We have further developed optogenetic approaches to manipulate bacterial gene expression and metabolite production inside the gut of live organisms, in order to investigate the microbiome-mitochondria communication in time and space. Our studies demonstrate a novel mode of signaling communication between bacteria and mitochondria, reveal its vital impacts on host healthy aging, and provide new methods to decipher the spatiotemporal relationship between the microbiome and the host.
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Mishra, Prashant, i David C. Chan. "Metabolic regulation of mitochondrial dynamics". Journal of Cell Biology 212, nr 4 (8.02.2016): 379–87. http://dx.doi.org/10.1083/jcb.201511036.
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Mitochondria are renowned for their central bioenergetic role in eukaryotic cells, where they act as powerhouses to generate adenosine triphosphate from oxidation of nutrients. At the same time, these organelles are highly dynamic and undergo fusion, fission, transport, and degradation. Each of these dynamic processes is critical for maintaining a healthy mitochondrial population. Given the central metabolic function of mitochondria, it is not surprising that mitochondrial dynamics and bioenergetics reciprocally influence each other. We review the dynamic properties of mitochondria, with an emphasis on how these processes respond to cellular signaling events and how they affect metabolism.
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Whelan, Sean P., i Brian S. Zuckerbraun. "Mitochondrial Signaling: Forwards, Backwards, and In Between". Oxidative Medicine and Cellular Longevity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/351613.
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Mitochondria are semiautonomous organelles that are a defining characteristic of almost all eukaryotic cells. They are vital for energy production, but increasing evidence shows that they play important roles in a wide range of cellular signaling and homeostasis. Our understanding of nuclear control of mitochondrial function has expanded over the past half century with the discovery of multiple transcription factors and cofactors governing mitochondrial biogenesis. More recently, nuclear changes in response to mitochondrial messaging have led to characterization of retrograde mitochondrial signaling, in which mitochondria have the ability to alter nuclear gene expression. Mitochondria are also integral to other components of stress response or quality control including ROS signaling, unfolded protein response, mitochondrial autophagy, and biogenesis. These avenues of mitochondrial signaling are discussed in this review.
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Porter, Susannah M. "Insights into eukaryogenesis from the fossil record". Interface Focus 10, nr 4 (12.06.2020): 20190105. http://dx.doi.org/10.1098/rsfs.2019.0105.
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Eukaryogenesis—the process by which the eukaryotic cell emerged—has long puzzled scientists. It has been assumed that the fossil record has little to say about this process, in part because important characters such as the nucleus and mitochondria are rarely preserved, and in part because the prevailing model of early eukaryotes implies that eukaryogenesis occurred before the appearance of the first eukaryotes recognized in the fossil record. Here, I propose a different scenario for early eukaryote evolution than is widely assumed. Rather than crown group eukaryotes originating in the late Paleoproterozoic and remaining ecologically minor components for more than half a billion years in a prokaryote-dominated world, I argue for a late Mesoproterozoic origin of the eukaryotic crown group, implying that eukaryogenesis can be studied using the fossil record. I review the proxy records of four crown group characters: the capacity to form cysts as evidenced by the presence of excystment structures; a complex cytoskeleton as evidenced by spines or pylomes; sterol synthesis as evidenced by steranes; and aerobic respiration—and therefore mitochondria—as evidenced by eukaryotes living in oxic environments, and argue that it might be possible to use these proxy records to infer the order in which these characters evolved. The records indicate that both cyst formation and a complex cytoskeleton appeared by late Paleoproterozoic time, and sterol synthesis appeared in the late Mesoproterozioc or early Neoproterozoic. The origin of aerobic respiration cannot as easily be pinned down, but current evidence permits the possibility that it evolved sometime in the Mesoproterozoic.
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Embley, T. Martin, Mark van der Giezen, David Horner, Patricia Dyal, Samantha Bell i Peter Foster. "Hydrogenosomes, Mitochondria and Early Eukaryotic Evolution". IUBMB Life (International Union of Biochemistry and Molecular Biology: Life) 55, nr 7 (1.07.2003): 387–95. http://dx.doi.org/10.1080/15216540310001592834.
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Pearce, Xavier G., Sarah J. Annesley i Paul R. Fisher. "The Dictyostelium model for mitochondrial biology and disease". International Journal of Developmental Biology 63, nr 8-9-10 (2019): 497–508. http://dx.doi.org/10.1387/ijdb.190233pf.
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The unicellular slime mould Dictyostelium discoideum is a valuable eukaryotic model organism in the study of mitochondrial biology and disease. As a member of the Amoebozoa, a sister clade to the animals and fungi, Dictyostelium mitochondrial biology shares commonalities with these organisms, but also exhibits some features of plants. As such it has made significant contributions to the study of eukaryotic mitochondrial biology. This review provides an overview of the advances in mitochondrial biology made by the study of Dictyostelium and examines several examples where Dictyostelium has and will contribute to the understanding of mitochondrial disease. The study of Dictyostelium’s mitochondrial biology has contributed to the understanding of mitochondrial genetics, transcription, protein import, respiration, morphology and trafficking, and the role of mitochondria in cellular differentiation. Dictyostelium is also proving to be a versatile model organism in the study both of classical mitochondrial disease e.g. Leigh syndrome, and in mitochondria-associated neurodegenerative diseases like Parkinson’s disease. The study of mitochondrial diseases presents a unique challenge due to the cryptic nature of their genotype-phenotype relationship. The use of Dictyostelium can contribute to resolving this problem by providing a genetically tractable, haploid eukaryotic organism with a suite of readily characterised phenotype readouts of cellular signalling pathways. Dictyostelium has provided insight into the signalling pathways involved in multiple neurodegenerative diseases and will continue to provide a significant contribution to the understanding of mitochondrial biology and disease.