Evidence map›Paper›PMID 9570323›Full record

ArticleRNA (New York, N.Y.)1998

Construction of an in vivo-regulated U6 snRNA transcription unit as a tool to study U6 function.

B G Luukkonen, B Séraphin

Open access · greenAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

B G LuukkonenEuropean Molecular Biology Laboratory, Heidelberg, Germany.
B Séraphin
European Molecular Biology Laboratory · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

U6 snRNA is the only spliceosomal snRNA transcribed by RNA polymerase III in yeast. We have constructed a regulated U6 snRNA transcription unit by introducing the binding site for the Escherichia coli lacI repressor protein in the U6 snRNA promoter. GAL-induced expression of lacI protein led to a decrease in U6 snRNA levels and blocked cell growth. lacI dissociation from the promoter, and consequent U6 snRNA transcription, could be induced by addition of IPTG and repression of lacI transcription. To test the usefulness of this system in studying spliceosomal U6 snRNA function, we conditionally expressed U6 snRNAs with a single base substitution in position A51. We demonstrate that expression of the U6-A51 mutations confers a strong dominant negative phenotype as shown by severe reductions in growth rate. In these strains, splicing of endogenous pre-mRNAs was blocked before the second step.

Indexed as

Escherichia coli ProteinsBacterial ProteinsBase SequenceBinding SitesDNA, RecombinantEscherichia coliGenes, FungalLac RepressorsMutationRepressor ProteinsRNA, Small NuclearRNA SplicingSaccharomyces cerevisiaeTranscription, GeneticBacterial ProteinsDNA, RecombinantEscherichia coli ProteinsLacI protein, E coliLac RepressorsRepressor ProteinsRNA, Small Nuclear

Identifiers

PMID9570323
PMCPMC1369612
OpenAlexW2101724452

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.