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Sökning: WFRF:(Trifunovic A)

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  • Trifunovic, A, et al. (författare)
  • Creation of mtDNA mutator mice
  • 2004
  • Ingår i: BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS. - 0005-2728. ; 1657, s. 21-21
  • Konferensbidrag (övrigt vetenskapligt)
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  • Bratic, Ivana, et al. (författare)
  • Mitochondrial DNA level, but not active replicase, is essential for Caenorhabditis elegans development
  • 2009
  • Ingår i: Nucleic Acids Research. - 0305-1048 .- 1362-4962. ; 37:6, s. 1817-1828
  • Tidskriftsartikel (refereegranskat)abstract
    • A number of studies showed that the development and the lifespan of Caenorhabditis elegans is dependent on mitochondrial function. In this study, we addressed the role of mitochondrial DNA levels and mtDNA maintenance in development of C. elegans by analyzing deletion mutants for mitochondrial polymerase gamma (polg-1(ok1548)). Surprisingly, even though previous studies in other model organisms showed necessity of polymerase gamma for embryonic development, homozygous polg-1(ok1548) mutants had normal development and reached adulthood without any morphological defects. However, polg-1 deficient animals have a seriously compromised gonadal function as a result of severe mitochondrial depletion, leading to sterility and shortened lifespan. Our results indicate that the gonad is the primary site of mtDNA replication, whilst the mtDNA of adult somatic tissues mainly stems from the developing embryo. Furthermore, we show that the mtDNA copy number shows great plasticity as it can be almost tripled as a response to the environmental stimuli. Finally, we show that the mtDNA copy number is an essential limiting factor for the worm development and therefore, a number of mechanisms set to maintain mtDNA levels exist, ensuring a normal development of C. elegans even in the absence of the mitochondrial replicase.
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  • Edgar, Daniel, et al. (författare)
  • Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice.
  • 2009
  • Ingår i: Cell metabolism. - 1932-7420. ; 10:2, s. 131-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The mtDNA mutator mice have high levels of point mutations and linear deletions of mtDNA causing a progressive respiratory chain dysfunction and a premature aging phenotype. We have now performed molecular analyses to determine the mechanism whereby these mtDNA mutations impair respiratory chain function. We report that mitochondrial protein synthesis is unimpaired in mtDNA mutator mice consistent with the observed minor alterations of steady-state levels of mitochondrial transcripts. These findings refute recent claims that circular mtDNA molecules with large deletions are driving the premature aging phenotype. We further show that the stability of several respiratory chain complexes is severely impaired despite normal synthesis of the corresponding mtDNA-encoded subunits. Our findings reveal a mechanism for induction of aging phenotypes by demonstrating a causative role for amino acid substitutions in mtDNA-encoded respiratory chain subunits, which, in turn, leads to decreased stability of the respiratory chain complexes and respiratory chain deficiency.
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  • Resultat 1-10 av 42
  • [1]2345Nästa
 
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