Evidence map›Paper›PMID 20107520›Full record

ArticlePLoS genetics2010

Nonsense-mediated decay enables intron gain in Drosophila.

Ashley Farlow, Eshwar Meduri, Marlies Dolezal, Liushuai Hua, Christian Schlötterer

Abstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. Functional Characterization of SMG7 Paralogs inFrontiers in plant science · 2018
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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

5 authors.

Ashley FarlowInstitut für Populationsgenetik, Veterinärmedizinische Universität Wien, Wien, Austria.
Eshwar Meduri
Marlies Dolezal
Liushuai Hua
Christian Schlötterer

Funding

Austrian Science Fund FWF L 403Austrian Science Fund FWF P 19832
6 · The paper itself

Abstract

Intron number varies considerably among genomes, but despite their fundamental importance, the mutational mechanisms and evolutionary processes underlying the expansion of intron number remain unknown. Here we show that Drosophila, in contrast to most eukaryotic lineages, is still undergoing a dramatic rate of intron gain. These novel introns carry significantly weaker splice sites that may impede their identification by the spliceosome. Novel introns are more likely to encode a premature termination codon (PTC), indicating that nonsense-mediated decay (NMD) functions as a backup for weak splicing of new introns. Our data suggest that new introns originate when genomic insertions with weak splice sites are hidden from selection by NMD. This mechanism reduces the sequence requirement imposed on novel introns and implies that the capacity of the spliceosome to recognize weak splice sites was a prerequisite for intron gain during eukaryotic evolution.

Indexed as

Codon, NonsenseIntronsAmino Acid SequenceAnimalsDrosophilaDrosophila ProteinsMolecular Sequence DataRNA SplicingSequence AlignmentSpliceosomesCodon, NonsenseDrosophila Proteins

Identifiers

PMID20107520
PMCPMC2809761

What OpenQuestion holds

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Registered trials

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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.