Mechanisms of mitochondrial DNA escape to the nucleus in the yeast Saccharomyces cerevisiae

Shafer, Karen S.; Hanekamp, Theodor; White, Karen H.; Thorsness, Peter E.

doi:10.1007/s002940050489

Cited by 42 publications

(37 citation statements)

References 47 publications

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“…Thorsness and colleagues used a unique assay for the escape of mitochondrial genes into the nucleus to demonstrate a requirement for vacuolar proteases. Since they were also able to show that the process is cell-autonomous, i.e., does not proceed via cell lysis and uptake of mitochondrial DNA into neighboring cells (104), these data are consistent with the contention that autophagy is a major regulated pathway for mitochondrial breakdown (16). The fact that mutants that compromise mitochondrial function also increase mitochondrial DNA escape into the nucleus also suggests that defective mitochondria are selectively targeted.…”

Section: Mitochondrial Recyclingsupporting

confidence: 75%

Autophagy in Yeast: Mechanistic Insights and Physiological Function

Abeliovich

Klionsky

2001

Microbiol Mol Biol Rev

163

135

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Unicellular eukaryotic organisms must be capable of rapid adaptation to changing environments. While such changes do not normally occur in the tissues of multicellular organisms, developmental and pathological changes in the environment of cells often require adaptation mechanisms not dissimilar from those found in simpler cells. Autophagy is a catabolic membrane-trafficking phenomenon that occurs in response to dramatic changes in the nutrients available to yeast cells, for example during starvation or after challenge with rapamycin, a macrolide antibiotic whose effects mimic starvation. Autophagy also occurs in animal cells that are serum starved or challenged with specific hormonal stimuli. In macroautophagy, the form of autophagy commonly observed, cytoplasmic material is sequestered in double-membrane vesicles called autophagosomes and is then delivered to a lytic compartment such as the yeast vacuole or mammalian lysosome. In this fashion, autophagy allows the degradation and recycling of a wide spectrum of biological macromolecules. While autophagy is induced only under specific conditions, salient mechanistic aspects of autophagy are functional in a constitutive fashion. In Saccharomyces cerevisiae, induction of autophagy subverts a constitutive membrane-trafficking mechanism called the cytoplasm-to-vacuole targeting pathway from a specific mode, in which it carries the resident vacuolar hydrolase, aminopeptidase I, to a nonspecific bulk mode in which significant amounts of cytoplasmic material are also sequestered and recycled in the vacuole. The general aim of this review is to focus on insights gained into the mechanism of autophagy in yeast and also to review our understanding of the physiological significance of autophagy in both yeast and higher organisms

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Section: Mitochondrial Recyclingsupporting

confidence: 75%

Autophagy in Yeast: Mechanistic Insights and Physiological Function

Abeliovich

Klionsky

2001

Microbiol Mol Biol Rev

163

135

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“…29,30 Furthermore, in yeast, impairment of the Yme1p-mediated degradation of Cox2p subunits that are not correctly assembled in cytochrome c oxidase complex of the respiratory chain, leads to mitochondrial degradation by a poorly characterised process. 31,32 As already stated, Dfmc1 cells grown at nonpermissive temperature are known to accumulate a-F1 and b-F1 aggregates in the mitochondrial matrix. 22 A tempting hypothesis would, therefore, be that the autophagic process depicted here could result from a similar signalling initiated by these matricial aggregates.…”

Section: Resultsmentioning

confidence: 81%

Impairing the bioenergetic status and the biogenesis of mitochondria triggers mitophagy in yeast

et al. 2005

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Autophagy, a highly regulated programme found in almost all eukaryotes, is mainly viewed as a catabolic process that degrades nonessential cellular components into molecular building blocks, subsequently available for biosynthesis at a lesser expense than de novo synthesis. Autophagy is largely known to be regulated by nutritional conditions. Here we show that, in yeast cells grown under nonstarving conditions, autophagy can be induced by mitochondrial dysfunction. Electron micrographs and biochemical studies show that an autophagic activity can result from impairing the mitochondrial electrochemical transmembrane potential. Furthermore, mitochondrial damage-induced autophagy results in the preferential degradation of impaired mitochondria (mitophagy), before leading to cell death. Mitophagy appears to rely on classical macroautophagy machinery while being independent of cellular ATP collapse. These results suggest that in this case, autophagy can be envisioned either as a process of mitochondrial quality control, or as an ultimate cellular response triggered when cells are overwhelmed with damaged mitochondria.

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“…These studies showed that (i) any segment of an organellar genome can be transferred to the nucleus, and (ii) that large norgDNAs exist that span several genes or even entire organellar chromosomes [6,7,14,15,22,25,26]. Moreover, analysis of human NUMTs has provided no evidence for splicing or polyadenylation of organellar nucleic acids before insertion [14], indicating that migration of mtDNA sequences to the nucleus is predominantly DNA mediated.…”

Section: Genomic Organization Of Norgdnasmentioning

confidence: 99%