Evidence map›Paper›PMID 29719607›Full record

ArticleOncotarget2018

Endonuclease G promotes mitochondrial genome cleavage and replication.

Rahel Stefanie Wiehe, Boris Gole, Laurent Chatre, Paul Walther, Enrico Calzia, Miria Ricchetti, Lisa Wiesmüller

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  8. Review
  9. Article
  10. Article
  11. Article
  12. Mitochondrial Factors in the Cell Nucleus.International journal of molecular sciences · 2023
    Review
  13. Apoptotic proteins with non-apoptotic activity: expression and function in cancer.Apoptosis : an international journal on programmed cell death · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mutagenic Consequences of Sublethal Cell Death Signaling.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Rahel Stefanie WieheDepartment of Obstetrics and Gynecology, Ulm University, Ulm, 89075, Germany.
Boris GoleDepartment of Obstetrics and Gynecology, Ulm University, Ulm, 89075, Germany.
Laurent ChatreDepartment of Developmental and Stem Cell Biology, Institute Pasteur, Stem Cells and Development, 75724 Cedex 15, Paris, France.
Paul WaltherCentral Facility for Electron Microscopy, Ulm University, Ulm, 89081, Germany.
Enrico CalziaInstitute of Anesthesiological Pathophysiology and Process Engineering, Ulm University Hospital, Ulm, 89081, Germany.
Miria RicchettiDepartment of Developmental and Stem Cell Biology, Institute Pasteur, Stem Cells and Development, 75724 Cedex 15, Paris, France.
Lisa WiesmüllerDepartment of Obstetrics and Gynecology, Ulm University, Ulm, 89075, Germany.
Universität Ulm · DECentre National de la Recherche Scientifique · FRUniversity Hospital Ulm · DEUniversity of Maribor · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endonuclease G (EndoG) is a nuclear-encoded endonuclease, mostly localised in mitochondria. In the nucleus EndoG participates in site-specific cleavage during replication stress and genome-wide DNA degradation during apoptosis. However, the impact of EndoG on mitochondrial DNA (mtDNA) metabolism is poorly understood. Here, we investigated whether EndoG is involved in the regulation of mtDNA replication and removal of aberrant copies. We applied the single-cell mitochondrial Transcription and Replication Imaging Protocol (mTRIP) and PCR-based strategies on human cells after knockdown/knockout and re-expression of EndoG. Our analysis revealed that EndoG stimulates both mtDNA replication initiation and mtDNA depletion, the two events being interlinked and dependent on EndoG's nuclease activity. Stimulation of mtDNA replication by EndoG was independent of 7S DNA processing at the replication origin. Importantly, both mtDNA-directed activities of EndoG were promoted by oxidative stress. Inhibition of base excision repair (BER) that repairs oxidative stress-induced DNA damage unveiled a pronounced effect of EndoG on mtDNA removal, reminiscent of recently discovered links between EndoG and BER in the nucleus. Altogether with the downstream effects on mitochondrial transcription, protein expression, redox status and morphology, this study demonstrates that removal of damaged mtDNA by EndoG and compensatory replication play a critical role in mitochondria homeostasis.

Indexed as

base excision repairendonuclease Gmitochondrial DNA degradationoxidative damage

Identifiers

PMID29719607
PMCPMC5915074
OpenAlexW2795492341

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.