Evidence map›Paper›PMID 21911497›Full record

ArticleThe Journal of biological chemistry2011

Uncoupling the roles of the SUV3 helicase in maintenance of mitochondrial genome stability and RNA degradation.

Xuning Emily Guo, Chi-Fen Chen, Dennis Ding-Hwa Wang, Aram Sandaldjian Modrek, Vy Hoai Phan, Wen-Hwa Lee, Phang-Lang Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. [SUV3 knockdown inhibits proliferation, migration, and invasion of hepatocellular carcinoma cells and induces PD-L1 expression].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024
    Article
  5. Article
  6. Molecular and cellular biology · 2021
    Article
  7. Article
  8. Article
  9. Human mitochondrial degradosome prevents harmful mitochondrial R loops and mitochondrial genome instability.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Xuning Emily GuoDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Chi-Fen ChenDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Dennis Ding-Hwa WangDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Aram Sandaldjian ModrekDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Vy Hoai PhanDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Wen-Hwa LeeDepartment of Biological Chemistry, University of California, Irvine, California 92697. Electronic address: whlee@uci.edu.
Phang-Lang ChenDepartment of Biological Chemistry, University of California, Irvine, California 92697. Electronic address: plchen@uci.edu.
University of California, Irvine · US

Funding

Mitochondrial Roles of the SUV3 in Premature Aging and CancerR01AG027877 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LEE, WEN-HWA · 2008 to 2012
$1.5M
Translational Research in Cancer Genomic MedicineT32CA113265 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI LEE, WEN-HWA · 2007 to 2011
$1.4M
BLRD VA IK2 BX006111NCI NIH HHS T32 CA113265NIA NIH HHS AG027877NIA NIH HHS R01 AG027877
6 · The paper itself

Abstract

Yeast SUV3 is a nuclear encoded mitochondrial RNA helicase that complexes with an exoribonuclease, DSS1, to function as an RNA degradosome. Inactivation of SUV3 leads to mitochondrial dysfunctions, such as respiratory deficiency; accumulation of aberrant RNA species, including excised group I introns; and loss of mitochondrial DNA (mtDNA). Although intron toxicity has long been speculated to be the major reason for the observed phenotypes, direct evidence to support or refute this theory is lacking. Moreover, it remains unknown whether SUV3 plays a direct role in mtDNA maintenance independently of its degradosome activity. In this paper, we address these questions by employing an inducible knockdown system in Saccharomyces cerevisiae with either normal or intronless mtDNA background. Expressing mutants defective in ATPase (K245A) or RNA binding activities (V272L or ΔCC, which carries an 8-amino acid deletion at the C-terminal conserved region) resulted in not only respiratory deficiencies but also loss of mtDNA under normal mtDNA background. Surprisingly, V272L, but not other mutants, can rescue the said deficiencies under intronless background. These results provide genetic evidence supporting the notion that the functional requirements of SUV3 for degradosome activity and maintenance of mtDNA stability are separable. Furthermore, V272L mutants and wild-type SUV3 associated with an active mtDNA replication origin and facilitated mtDNA replication, whereas K245A and ΔCC failed to support mtDNA replication. These results indicate a direct role of SUV3 in maintaining mitochondrial genome stability that is independent of intron turnover but requires the intact ATPase activity and the CC conserved region.

Indexed as

Adenosine TriphosphateCodonConserved SequenceDEAD-box RNA HelicasesGenome, MitochondrialIntronsMembrane PotentialsMitochondriaMutationRNARNA HelicasesRNA StabilitySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAdenosine TriphosphateCodonDEAD-box RNA HelicasesRNARNA HelicasesSaccharomyces cerevisiae ProteinsSUV3 protein, S cerevisiae

Identifiers

PMID21911497
PMCPMC3207411
OpenAlexW2048103232

What OpenQuestion holds

Textmetadata
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.