Cited by 17

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

iPSC culture expansion selects against putatively actionable mutations in the mitochondrial genome

Kosanke, Maike, Davenport, Colin, Szepes, Monika, Wiehlmann, Lutz, Kohrn, Tim, Dorda, Marie, Gruber, Jonas, Menge, Kaja, Sievert, Maike, Melchert, Anna, Gruh, Ina, Göhring, Gudrun, Martin, Ulrich·2021·Stem Cell Reports

Published version of a preprint

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.stemcr.2021.08.016

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Individual PSCs display considerable heterogeneity in mutation loads that can impact their utilization in disease modeling and as drug screening platforms.

    “Furthermore, individual PSCs display considerable heterogeneity in mutation loads that can impact their utilization in disease modeling and as drug screening platforms [163,164].”

    From The Mitochondrial Genome in Aging and Disease and the Future of Mitochondrial Therapeutics (2022) · cites this paper as [164]

    The Introduction and Results report differing mitochondrial variants and heteroplasmy levels among iPSC clones, including potentially damaging variants. The Discussion says heteroplasmy levels can rise enough to affect cell functionality. Our copy does not establish an impact on using those cells for disease modeling or drug screening; “drug screening” appears only in a reference title. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 48

  1. Afgan, 2018, The Galaxy platform for accessible, reproducible and collaborative biomedical analyses: 2018 update, Nucleic Acids Res., 46, W537, 10.1093/nar/gky379 · DOI · Paper page
  2. Andrews, 2017, Assessing the safety of human pluripotent stem cells and their derivatives for clinical applications, Stem Cell Reports, 9, 1, 10.1016/j.stemcr.2017.05.029 · DOI
  3. Aryaman, 2019, Mitochondrial network state scales mtDNA genetic dynamics, Genetics, 212, 1429, 10.1534/genetics.119.302423 · DOI
  4. Bonora, 2019, Targeting mitochondria for cardiovascular disorders: therapeutic potential and obstacles, Nat. Rev. Cardiol., 16, 33, 10.1038/s41569-018-0074-0 · DOI
  5. Cao, 2009, New evidence confirms that the mitochondrial bottleneck is generated without reduction of mitochondrial DNA content in early primordial germ cells of mice, PLoS Genet., 5, e1000756, 10.1371/journal.pgen.1000756 · DOI
  6. Cherry, 2013, Induced pluripotent stem cells with a mitochondrial DNA deletion, Stem Cells, 31, 1287, 10.1002/stem.1354 · DOI
  7. Chinnery, 2019, De-fusing mitochondria defuses the mtDNA time-bomb, Cell Res., 29, 781, 10.1038/s41422-019-0206-z · DOI
  8. Clayton, 1991, Replication and transcription of vertebrate mitochondrial DNA, Annu. Rev. Cell Biol., 7, 453, 10.1146/annurev.cb.07.110191.002321 · DOI
  9. Copeland, 2002, Mitochondrial DNA alterations in cancer, Cancer Invest., 20, 557, 10.1081/CNV-120002155 · DOI
  10. Deuse, 2019, De novo mutations in mitochondrial DNA of iPSCs produce immunogenic neoepitopes in mice and humans, Nat. Biotechnol., 37, 1137, 10.1038/s41587-019-0227-7 · DOI
  11. Floros, 2018, Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos, Nat. Cell Biol., 20, 144, 10.1038/s41556-017-0017-8 · DOI
  12. Folmes, 2013, Disease-causing mitochondrial heteroplasmy segregated within induced pluripotent stem cell clones derived from a patient with MELAS, Stem Cells, 31, 1298, 10.1002/stem.1389 · DOI
  13. Haase, 2009, Generation of induced pluripotent stem cells from human cord blood, Cell Stem Cell, 5, 434, 10.1016/j.stem.2009.08.021 · DOI
  14. Halloin, 2019, Continuous WNT control enables advanced hPSC cardiac processing and prognostic surface marker identification in chemically defined suspension culture, Stem Cell Reports, 13, 366, 10.1016/j.stemcr.2019.06.004 · DOI
  15. Hamalainen, 2013, Tissue- and cell-type-specific manifestations of heteroplasmic mtDNA 3243A>G mutation in human induced pluripotent stem cell-derived disease model, Proc. Natl. Acad. Sci., 110, E3622, 10.1073/pnas.1311660110 · DOI
  16. Hung, 2016, Study of mitochondrial respiratory defects on reprogramming to human induced pluripotent stem cells, Aging (Albany NY), 8, 945, 10.18632/aging.100950 · DOI
  17. Kandul, 2016, Selective removal of deletion-bearing mitochondrial DNA in heteroplasmic Drosophila, Nat. Commun., 7, 13100, 10.1038/ncomms13100 · DOI
  18. Kang, 2016, Age-related accumulation of somatic mitochondrial DNA mutations in adult-derived human iPSCs, Cell Stem Cell, 18, 625, 10.1016/j.stem.2016.02.005 · DOI
  19. Kensah, 2011, A novel miniaturized multimodal bioreactor for continuous in situ assessment of bioartificial cardiac tissue during stimulation and maturation, Tissue Eng. Part C Methods, 17, 463, 10.1089/ten.tec.2010.0405 · DOI
  20. Kensah, 2013, Murine and human pluripotent stem cell-derived cardiac bodies form contractile myocardial tissue in vitro, Eur. Heart J., 34, 1134, 10.1093/eurheartj/ehs349 · DOI · Paper page
  21. Klein Gunnewiek, 2020, m.3243A > G-induced mitochondrial dysfunction impairs human neuronal development and reduces neuronal network activity and synchronicity, Cell Rep., 31, 107538, 10.1016/j.celrep.2020.107538 · DOI
  22. Kosanke, 2021, Reprogramming enriches for somatic cell clones with small scale mutations in cancer-associated genes, Mol. Ther., S1525-0016, 00194
  23. Kropp, 2016, Impact of feeding strategies on the scalable expansion of human pluripotent stem cells in single-use stirred tank bioreactors, Stem Cells Transl. Med., 5, 1289, 10.5966/sctm.2015-0253 · DOI
  24. Latorre-Pellicer, 2016, Mitochondrial and nuclear DNA matching shapes metabolism and healthy ageing, Nature, 535, 561, 10.1038/nature18618 · DOI · Paper page
  25. Laude, 2009, Compartmentalized signalling: Ca2+ compartments, microdomains and the many facets of Ca2+ signalling, FEBS J., 276, 1800, 10.1111/j.1742-4658.2009.06927.x · DOI
  26. Lieber, 2019, Mitochondrial fragmentation drives selective removal of deleterious mtDNA in the germline, Nature, 570, 380, 10.1038/s41586-019-1213-4 · DOI
  27. Ma, 2015, Atg5-independent autophagy regulates mitochondrial clearance and is essential for iPSC reprogramming, Nat. Cell Biol., 17, 1379, 10.1038/ncb3256 · DOI
  28. Maitra, 2005, Genomic alterations in cultured human embryonic stem cells, Nat. Genet., 37, 1099, 10.1038/ng1631 · DOI
  29. Mannhardt, 2020, Comparison of 10 control hPSC lines for drug screening in an engineered heart tissue format, Stem Cell Reports, 15, 983, 10.1016/j.stemcr.2020.09.002 · DOI
  30. McElhoe, 2014, Development and assessment of an optimized next-generation DNA sequencing approach for the mtgenome using the Illumina MiSeq, Forensic Sci. Int. Genet., 13, 20, 10.1016/j.fsigen.2014.05.007 · DOI
  31. McLaren, 2016, The Ensembl variant effect predictor, Genome Biol., 17, 122, 10.1186/s13059-016-0974-4 · DOI · Paper page
  32. Naue, 2015, Evidence for frequent and tissue-specific sequence heteroplasmy in human mitochondrial DNA, Mitochondrion, 20, 82, 10.1016/j.mito.2014.12.002 · DOI
  33. Park, 2011, Mitochondrial DNA mutations in disease and aging, J. Cell Biol., 193, 809, 10.1083/jcb.201010024 · DOI · Paper page
  34. Payne, 2013, Universal heteroplasmy of human mitochondrial DNA, Hum. Mol. Genet., 22, 384, 10.1093/hmg/dds435 · DOI
  35. Perales-Clemente, 2016, Natural underlying mtDNA heteroplasmy as a potential source of intra-person hiPSC variability, EMBO J., 35, 1979, 10.15252/embj.201694892 · DOI
  36. Preste, 2019, HmtVar: a new resource for human mitochondrial variations and pathogenicity data, Nucleic Acids Res., 47, D1202, 10.1093/nar/gky1024 · DOI
  37. Prigione, 2010, The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells, Stem Cells, 28, 721, 10.1002/stem.404 · DOI
  38. Prigione, 2011, Mitochondrial-associated cell death mechanisms are reset to an embryonic-like state in aged donor-derived iPS cells harboring chromosomal aberrations, PLoS One, 6, e27352, 10.1371/journal.pone.0027352 · DOI
  39. Roze, 2005, Germline bottlenecks, biparental inheritance and selection on mitochondrial variants: a two-level selection model, Genetics, 170, 1385, 10.1534/genetics.104.039495 · DOI
  40. Sercel, 2021, Mitochondrial DNA dynamics in reprogramming to pluripotency, Trends Cell Biol., 31, 311, 10.1016/j.tcb.2020.12.009 · DOI
  41. Shakiba, 2019, Cell competition during reprogramming gives rise to dominant clones, Science, 364, eaan0925, 10.1126/science.aan0925 · DOI
  42. Wahlestedt, 2014, Somatic cells with a heavy mitochondrial DNA mutational load render induced pluripotent stem cells with distinct differentiation defects, Stem Cells, 32, 1173, 10.1002/stem.1630 · DOI
  43. Wei, 2019, Germline selection shapes human mitochondrial DNA diversity, Science, 364, eaau6520, 10.1126/science.aau6520 · DOI
  44. Weissbein, 2014, Quality control: genome maintenance in pluripotent stem cells, J. Cell Biol., 204, 153, 10.1083/jcb.201310135 · DOI
  45. Weissensteiner, 2016, HaploGrep 2: mitochondrial haplogroup classification in the era of high-throughput sequencing, Nucleic Acids Res., 44, W58, 10.1093/nar/gkw233 · DOI
  46. Yokota, 2015, Mitochondrial respiratory dysfunction caused by a heteroplasmic mitochondrial DNA mutation blocks cellular reprogramming, Hum. Mol. Genet., 24, 4698, 10.1093/hmg/ddv201 · DOI
  47. Yoshihara, 2017, Hotspots of de novo point mutations in induced pluripotent stem cells, Cell Rep., 21, 308, 10.1016/j.celrep.2017.09.060 · DOI
  48. Zambelli, 2018, Random mutagenesis, clonal events, and embryonic or somatic origin determine the mtDNA variant type and load in human pluripotent stem cells, Stem Cell Reports., 11, 102, 10.1016/j.stemcr.2018.05.007 · DOI

Cited by

Sorted by citations

Metadata

Authors
Kosanke, M., Davenport, C., Szepes, M., Wiehlmann, L., Kohrn, T., Dorda, M., Gruber, J., Menge, K., Sievert, M., Melchert, A., Gruh, I., Göhring, G., & Martin, U.
Venue
Stem Cell Reports
Publisher
Elsevier BV
Published
2021-10
Volume
16
Issue
10
Pages
2488-2502
ISSN
2213-6711
Cited by
17
References
2
Language
en
Funders
  • Deutsches Zentrum für Lungenforschung (82DZL00401, 82DZL00201)
  • Lower Saxony State Ministry of Science and Culture
  • Bundesministerium für Bildung und Forschung
  • Deutsche Forschungsgemeinschaft

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review