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Cited by 96

The mtDNA mutation spectrum of the progeroid polg mutator mouse includes abundant control region multimers

Williams, Siôn L., Huang, Jia, Edwards, Yvonne J.K., Ulloa, Rick H., Dillon, Lloye M., Prolla, Tomas A., Vance, Jeffery M., Moraes, Carlos T., Züchner, Stephan·2010·Cell Metabolism
DOI 10.1016/j.cmet.2010.11.012PMC PMC3175596
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Crossref · 10.1016/j.cmet.2010.11.012

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  • Mouse models have been used to study comparable phenotypes due to mutations in nuclear-encoded proteins involved in mitochondrial biogenesis, such as TFAM, PolG, Twinkle, and SURF-1.

    “Mouse models have further been used to study comparable phenotypes due to mutations in nuclear-encoded proteins involved in mitochondrial biogenesis, such as TFAM [152], PolG [153], Twinkle [154,155,156], and SURF-1 [157].”

    From The Mitochondrial Genome in Aging and Disease and the Future of Mitochondrial Therapeutics (2022) · cites this paper as [153]

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Research works printed but not linked: 27

  1. Albring, 1977, Association of a protein structure of probable membrane derivation with HeLa cell mitochondrial DNA near its origin of replication, Proc. Natl. Acad. Sci. USA, 74, 1348, 10.1073/pnas.74.4.1348 · DOI
  2. Bailey, 2009, Mice expressing an error-prone DNA polymerase in mitochondria display elevated replication pausing and chromosomal breakage at fragile sites of mitochondrial DNA, Nucleic Acids Res., 37, 2327, 10.1093/nar/gkp091 · DOI
  3. Brockington, 1993, A tandem duplication in the D-loop of human mitochondrial DNA is associated with deletions in mitochondrial myopathies, Nat. Genet., 4, 67, 10.1038/ng0593-67 · DOI
  4. Brown, 2005, Replication of mitochondrial DNA occurs by strand displacement with alternative light-strand origins, not via a strand-coupled mechanism, Genes Dev., 19, 2466, 10.1101/gad.1352105 · DOI
  5. Edgar, 2009, Random point mutations with major effects on protein-coding genes are the driving force behind premature aging in mtDNA mutator mice, Cell Metab., 10, 131, 10.1016/j.cmet.2009.06.010 · DOI · Paper page
  6. Edgar, 2010, Response: Point Mutations Are Causing Progeroid Phenotypes in the mtDNA Mutator Mouse, Cell Metab., 11, 93, 10.1016/j.cmet.2009.12.006 · DOI
  7. Fukui, 2009, Mechanisms of formation and accumulation of mitochondrial DNA deletions in aging neurons, Hum. Mol. Genet., 18, 1028, 10.1093/hmg/ddn437 · DOI
  8. He, 2010, Heteroplasmic mitochondrial DNA mutations in normal and tumour cells, Nature, 464, 610, 10.1038/nature08802 · DOI
  9. Jin, 2001, The 3′—>5′ exonuclease of DNA polymerase delta can substitute for the 5′ flap endonuclease Rad27/Fen1 in processing Okazaki fragments and preventing genome instability, Proc. Natl. Acad. Sci. USA, 98, 5122, 10.1073/pnas.091095198 · DOI
  10. Johnson, 2001, Exonuclease proofreading by human mitochondrial DNA polymerase, J. Biol. Chem., 276, 38097, 10.1074/jbc.M106046200 · DOI
  11. Kasahara, 2006, Mice with neuron-specific accumulation of mitochondrial DNA mutations show mood disorder-like phenotypes, Mol. Psychiatry, 11, 577, 10.1038/sj.mp.4001824 · DOI
  12. Kraytsberg, 2009, Do mtDNA deletions drive premature aging in mtDNA mutator mice?, Aging Cell, 8, 502, 10.1111/j.1474-9726.2009.00484.x · DOI · Paper page
  13. Kujoth, 2005, Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging, Science, 309, 481, 10.1126/science.1112125 · DOI · Paper page
  14. Manfredi, 1995, High levels of mitochondrial DNA with an unstable 260-bp duplication in a patient with a mitochondrial myopathy, Neurology, 45, 762, 10.1212/WNL.45.4.762 · DOI
  15. Rudolph, 2009, Pathological replication in cells lacking RecG DNA translocase, Mol. Microbiol., 73, 352, 10.1111/j.1365-2958.2009.06773.x · DOI
  16. Rudolph, 2009, Replication fork collisions cause pathological chromosomal amplification in cells lacking RecG DNA translocase, Mol. Microbiol., 74, 940, 10.1111/j.1365-2958.2009.06909.x · DOI
  17. Sachadyn, 2008, Naturally occurring mitochondrial DNA heteroplasmy in the MRL mouse, Mitochondrion, 8, 358, 10.1016/j.mito.2008.07.007 · DOI
  18. Schaeffer, 2005, Protein—protein interactions in the eubacterial replisome, IUBMB Life, 57, 5, 10.1080/15216540500058956 · DOI
  19. Stewart, 2008, Strong purifying selection in transmission of mammalian mitochondrial DNA, PLoS Biol., 6, e10, 10.1371/journal.pbio.0060010 · DOI
  20. Torroni, 1994, mtDNA and the origin of Caucasians: identification of ancient Caucasian-specific haplogroups, one of which is prone to a recurrent somatic duplication in the D-loop region, Am. J. Hum. Genet., 55, 760
  21. Vasta, 2009, Next generation sequence analysis for mitochondrial disorders, Genome Med., 1, 100, 10.1186/gm100 · DOI
  22. Vermulst, 2008, DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice, Nat. Genet., 40, 392, 10.1038/ng.95 · DOI · Paper page
  23. Vermulst, 2009, On mitochondria, mutations, and methodology, Cell Metab., 10, 437, 10.1016/j.cmet.2009.11.001 · DOI
  24. Wai, 2008, The mitochondrial DNA genetic bottleneck results from replication of a subpopulation of genomes, Nat. Genet., 40, 1484, 10.1038/ng.258 · DOI
  25. Wei, 1996, Tandem duplications and large-scale deletions of mitochondrial DNA are early molecular events of human aging process, Ann. N Y Acad. Sci., 786, 82, 10.1111/j.1749-6632.1996.tb39054.x · DOI
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Cited by

Sorted by citations

Authors
Williams, S. L., Huang, J., Edwards, Y. J. K., Ulloa, R. H., Dillon, L. M., Prolla, T. A., Vance, J. M., Moraes, C. T., & Züchner, S.
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2010-12
Volume
12
Issue
6
Pages
675-682
ISSN
1550-4131
DOI
10.1016/j.cmet.2010.11.012
PMC
PMC3175596
Cited by
96
References
4
Language
en
Licence
Funders
  • Presbyterian Historical Society (AG036871, CA85700, EY10804, NS053767, P50NS071674)
  • United Mitochondrial Disease Foundation

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