Reversion of Endosymbiosis?

Krajčovič, Juraj; Ebringer, L.; Schwartzbach, Steven D.

doi:10.1007/0-306-48173-1_11

Cited by 11 publications

(16 citation statements)

References 133 publications

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“…This might be a reverse step to phylogenetic uptake of mitochondria according to the endosymbiotic theory. In yeast, the phenomenon of mitochondrial regression is connected to the petit phenotype and can be experimentally induced, which is then called rho status [ 28 , 29 ]. Physiologically, the mitochondrial turnover takes place via mitophagy, the specific autophagic elimination of mitochondria.…”

Section: Discussionmentioning

confidence: 99%

ATP Synthase Deficiency due to TMEM70 Mutation Leads to Ultrastructural Mitochondrial Degeneration and Is Amenable to Treatment

Braczynski

Vlaho

Müller

et al. 2015

BioMed Research International

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TMEM70 is involved in the biogenesis of mitochondrial ATP synthase and mutations in the TMEM70 gene impair oxidative phosphorylation. Herein, we report on pathology and treatment of ATP synthase deficiency in four siblings. A consanguineous family of Roma (Gipsy) ethnic origin gave birth to 6 children of which 4 were affected presenting with dysmorphic features, failure to thrive, cardiomyopathy, metabolic crises, and 3-methylglutaconic aciduria as clinical symptoms. Genetic testing revealed a homozygous mutation (c.317-2A>G) in the TMEM70 gene. While light microscopy was unremarkable, ultrastructural investigation of muscle tissue revealed accumulation of swollen degenerated mitochondria with lipid crystalloid inclusions, cristae aggregation, and exocytosis of mitochondrial material. Biochemical analysis of mitochondrial complexes showed an almost complete ATP synthase deficiency. Despite harbouring the same mutation, the clinical outcome in the four siblings was different. Two children died within 60 h after birth; the other two had recurrent life-threatening metabolic crises but were successfully managed with supplementation of anaplerotic amino acids, lipids, and symptomatic treatment during metabolic crisis. In summary, TMEM70 mutations can cause distinct ultrastructural mitochondrial degeneration and almost complete deficiency of ATP synthase but are still amenable to treatment.

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Section: Discussionmentioning

confidence: 99%

ATP Synthase Deficiency due to TMEM70 Mutation Leads to Ultrastructural Mitochondrial Degeneration and Is Amenable to Treatment

Braczynski

Vlaho

Müller

et al. 2015

BioMed Research International

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“…The N-succinimide derivate of ofloxacin induced a bleached mutant of E. gracilis W gm ZOflL with permanently altered mitochondria, some ≈5-8 μm long and wide having an unusual shape, others disfigured with unusual shape, giant swollen oval-shaped megamitochondria and some very long (50-60 μm) ones are also seen in addition to normal mitochondria (Polónyi et al 1998;Vacula et al 2001). E. gracilis amitochondrial cells are never found (Krajčovič et al 2002).…”

Section: Reductive Evolution Of Plastids In Euglenidsmentioning

confidence: 95%

“…Immunoblot analysis has detected the gene product of rbcL as the expected 53-kDa polypeptide (Gockel et al 1994). Detection of plastid-encoded proteins clearly indicates that the translational machinery in E. longa plastids is functional as expected if an E. longa plastid-encoded protein is required for cell growth and viability (for review see Krajčovič et al 2002).…”

Section: Reductive Evolution Of Plastids In Euglenidsmentioning

confidence: 97%

“…Papers on the bleaching phenomenon in the mixotrophic euglenoid flagellate E. gracilis have demonstrated that treatment with xenobiotics results in irreversible elimination of functional chloroplasts (Krajčovič et al 2002;Krajčovič 2005). Stable bleached mutants incapable of photosynthesis exist that can grow heterotrophically; e.g., the stable bleached mutant W 3 BUL contains a stigma and also a plastid remnant with thylakoid-membrane-specific sulfolipid, while the stable mutant W 10 SmL lacks detectable carotenoids, sulfolipids, stigma and even an identifiable plastid remnant (Schiff et al 1971;Krajčovič et al 2002).…”

Section: Reductive Evolution Of Plastids In Euglenidsmentioning

confidence: 99%

“…Stable bleached mutants incapable of photosynthesis exist that can grow heterotrophically; e.g., the stable bleached mutant W 3 BUL contains a stigma and also a plastid remnant with thylakoid-membrane-specific sulfolipid, while the stable mutant W 10 SmL lacks detectable carotenoids, sulfolipids, stigma and even an identifiable plastid remnant (Schiff et al 1971;Krajčovič et al 2002). The N-succinimide derivate of ofloxacin induced a bleached mutant of E. gracilis W gm ZOflL with permanently altered mitochondria, some ≈5-8 μm long and wide having an unusual shape, others disfigured with unusual shape, giant swollen oval-shaped megamitochondria and some very long (50-60 μm) ones are also seen in addition to normal mitochondria (Polónyi et al 1998;Vacula et al 2001).…”

Section: Reductive Evolution Of Plastids In Euglenidsmentioning

confidence: 99%

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On the origin of chloroplasts, import mechanisms of chloroplast-targeted proteins, and loss of photosynthetic ability — review

2009

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Primary plastids of green algae (including land plants), red algae and glaucophytes are bounded by two membranes and are thought to be derived from a single primary endosymbiosis of a cyanobacterium in a eukaryotic host. Complex plastids of euglenids and chlorarachneans bounded by three and four membranes, respectively, most likely arose via two separate secondary endosymbioses of a green alga in a eukaryotic host. Secondary plastids of cryptophyta, haptophyta, heterokontophyta and apicomplexan parasites bounded by four membranes, and plastids of dinoflagellates bounded by three membranes could have arisen via a single secondary endosymbiosis of a red alga in a eukaryotic host (chromalveolate hypothesis). However, the scenario of separate tertiary origins (symbioses of an alga possessing secondary plastids in a eukaryotic host) of some (or even most) chromalveolate plastids can be also consistent with the current data. The protein import into complex plastids differs from the import into primary plastids, as complex plastids contain one or two extra membrane(s). In organisms with primary plastids, plastid-targeted proteins contain N-terminal transit peptide which ferries proteins through the protein import machineries (multiprotein complexes) of the two (originally cyanobacterial) membranes. In organisms with complex plastids, the secretory signal sequence directing proteins to endomembrane system and afterwards through extra outermost membrane(s) is generally present upstream of the classical transit peptide. Several free-living as well as parasitic eukaryotes possess non-photosynthetic plastids. These plastids have generally retained the plastid genome, functional plastid transcriptional and translational apparatus, and various metabolic pathways, suggesting that though these plastids lost their photosynthetic ability, they are essential for the mentioned organisms. Nevertheless, some eukaryotes could have lost chloroplast compartment completely.

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