Evidence map›Paper›PMID 14612420›Full record

ArticleMolecular and cellular biology2003

The DIVa maturase binding site in the yeast group II intron aI2 is essential for intron homing but not for in vivo splicing.

Hon-Ren Huang, Michael Y Chao, Barbara Armstrong, Yong Wang, Alan M Lambowitz, Philip S Perlman

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Group II introns: mobile ribozymes that invade DNA.Cold Spring Harbor perspectives in biology · 2011
    Review
  8. Article
  9. Article
  10. Article
  11. The splicing of yeast mitochondrial group I and group II introns requires a DEAD-box protein with RNA chaperone function.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  12. Article
  13. Article
  14. Article
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

6 authors at 2 institutions in 1 country.

Hon-Ren HuangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA.
Michael Y Chao
Barbara Armstrong
Yong Wang
Alan M Lambowitz
Philip S Perlman
The University of Texas Southwestern Medical Center · USThe University of Texas at Austin · US

Funding

TRAINING IN CARDIOVASCULAR RESEARCHT32HL007360 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HILL, JOSEPH A · 1985 to 2012
$11.8M
RNA SPLICING IN NEUROSPORA MITOCHONDRIAR01GM037951 · NIGMS · UNIVERSITY OF TEXAS AUSTIN · PI LAMBOWITZ, ALAN M. · 1986 to 2016
$6.6M
GENETIC AND MOLECULAR STUDIES OF RNA SPLICINGR01GM031480 · NIGMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BUTOW, RONALD A · 1985 to 2004
$1.8M
INVOLVEMENT OF PROTEINS IN SPLICING GROUP I INTRONSR37GM037951 · NIGMS · UNIVERSITY OF TEXAS AUSTIN · PI LAMBOWITZ, ALAN M. · 1993 to 2002
$1.2M
NHLBI NIH HHS T32 HL007360NHLBI NIH HHS T32-HL07360NIGMS NIH HHS GM31480NIGMS NIH HHS GM37951NIGMS NIH HHS R01 GM031480NIGMS NIH HHS R01 GM037951NIGMS NIH HHS R37 GM037951
6 · The paper itself

Abstract

Splicing of the Saccharomyces cerevisiae mitochondrial DNA group II intron aI2 depends on the intron-encoded 62-kDa reverse transcriptase-maturase protein (p62). In wild-type strains, p62 remains associated with the excised intron lariat RNA in ribonucleoprotein (RNP) particles that are essential for intron homing. Studies of a bacterial group II intron showed that the DIVa substructure of intron domain IV is a high-affinity binding site for its maturase. Here we first present in vitro evidence extending that conclusion to aI2. Then, experiments with aI2 DIVa mutant strains show that the binding of p62 to DIVa is not essential for aI2 splicing in vivo but is essential for homing. Because aI2 splicing in the DIVa mutant strains remains maturase dependent, splicing must rely on other RNA-protein contacts. The p62 that accumulates in the mutant strains has reverse transcriptase activity, but fractionation experiments at high and low salt concentrations show that it associates more weakly than the wild-type protein with endogenous mitochondrial RNAs, and that phenotype probably explains the homing defect. Replacing the DIVa of aI2 with that of the closely related intron aI1 improves in vivo splicing but not homing, indicating that DIVa contributes to the specificity of the maturase-RNA interaction needed for homing.

Indexed as

IntronsBase SequenceBinding SitesDNA, FungalDNA, MitochondrialGenetic Complementation TestMolecular Sequence DataMutationNucleic Acid ConformationOpen Reading FramesRNARNA-Directed DNA PolymeraseRNA, FungalRNA, MitochondrialRNA SplicingSaccharomyces cerevisiaeaI2 protein, S cerevisiaeDNA, FungalDNA, MitochondrialRNARNA-Directed DNA PolymeraseRNA, FungalRNA, MitochondrialSaccharomyces cerevisiae Proteins

Identifiers

PMID14612420
PMCPMC262681
OpenAlexW2126456230

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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.