Evidence map›Paper›PMID 10581262›Full record

ArticleGenetics1999

Intron homing with limited exon homology. Illegitimate double-strand-break repair in intron acquisition by phage t4.

M M Parker, M Belisle, M Belfort

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Insertion of a homing endonuclease creates a genes-in-pieces ribonucleotide reductase that retains function.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  10. Article
  11. Barriers to intron promiscuity in bacteria.Journal of bacteriology · 2000
    Review
  12. 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

3 authors at 1 institution in 1 country.

M M ParkerMolecular Genetics Program, Wadsworth Center, New York State Department of Health and School of Public Health, State University of New York, Albany, New York 12201-2002, USA.
M Belisle
M Belfort
New York State Department of Health · US

Funding

SELF-SPLICING INTEINS: FUNCTION, EVOLUTION, APPLICATIONR01GM044844 · NIGMS · WADSWORTH CENTER · PI BELFORT, MARLENE · 1990 to 2019
$8.9M
SELF-SPLICING INTRONS IN THE PHAGE T4/E COLI SYSTEMR01GM039422 · NIGMS · WADSWORTH CENTER · PI BELFORT, MARLENE · 1988 to 2019
$5.3M
INTRON DYNAMICS IN BACTERIAR37GM039422 · NIGMS · WADSWORTH CENTER · PI BELFORT, MARLENE · 2001 to 2010
$4.0M
NIGMS NIH HHS GM-39422NIGMS NIH HHS GM-44844
6 · The paper itself

Abstract

The td intron of bacteriophage T4 encodes a DNA endonuclease that initiates intron homing to cognate intronless alleles by a double-strand-break (DSB) repair process. A genetic assay was developed to analyze the relationship between exon homology and homing efficiency. Because models predict exonucleolytic processing of the cleaved recipient leading to homologous strand invasion of the donor allele, the assay was performed in wild-type and exonuclease-deficient (rnh or dexA) phage. Efficient homing was supported by exon lengths of 50 bp or greater, whereas more limited exon lengths led to a precipitous decline in homing levels. However, extensive homology in one exon still supported elevated homing levels when the other exon was completely absent. Analysis of these "one-sided" events revealed recombination junctions at ectopic sites of microhomology and implicated nucleolytic degradation in illegitimate DSB repair in T4. Interestingly, homing efficiency with extremely limiting exon homology was greatly elevated in phage deficient in the 3'-5' exonuclease, DexA, suggesting that the length of 3' tails is a major determinant of the efficiency of DSB repair. Together, these results suggest that illegitimate DSB repair may provide a means by which introns can invade ectopic sites.

Indexed as

DNA DamageDNA RepairExonsIntronsBacteriophage T4Base SequenceDNA, ViralEndodeoxyribonucleasesEscherichia coliMolecular Sequence DataSequence Homology, Nucleic AcidDNA, ViralEndodeoxyribonucleasesI-TEVI endonuclease

Identifiers

PMID10581262
PMCPMC1460845
OpenAlexW2135003224

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.