Evidence map›Paper›PMID 7753636›Full record

ArticleNucleic acids research1995

INO1-100: an allele of the Saccharomyces cerevisiae INO1 gene that is transcribed without the action of the positive factors encoded by the INO2, INO4, SWI1, SWI2 and SWI3 genes.

S Swift, P McGraw

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Article in Nucleic acids research, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

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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

7 citing papers in PubMed, 18 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.

S SwiftDepartment of Biological Sciences, University of Maryland (UMBC), Catonsville 21228, USA.
P McGraw

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A dominant allele of the INO1 locus, INO1-100, does not require the positive regulators encoded by INO2 and INO4 for expression. Sequence analysis showed that INO1-100 had a 239 bp deletion in the INO1 promoter. INO1-100 suppressed the inositol auxotrophy of ino2, ino4, swi1, swi2 and swi3 mutants. Transcription of INO1-100 was constitutive and independent of these regulators. A 20 bp deletion from -247 to -228 caused a similar phenotype. A 38 bp deletion from -245 to -208 suppressed the inositol auxotrophy of an ino2 mutant, but not an ino4 mutant, indicating that Ino2p and Ino4p may function alone as well as in a complex. A 40 bp deletion from -287 to -248 that removed a URS1 site caused constitutive transcription that required INO2 and INO4. A deletion from -167 to -128 suppressed the inositol auxotrophy of swi, ino2 and ino4 mutants, indicating the presence of a previously unidentified URS1. Mutation of the specific negative regulator of phospholipid synthesis encoded by OPI1 suppressed the inositol auxotrophy of swi2 mutants. This study indicates that negative regulation of INO1 is chromatin mediated and provides in vivo information on the interaction of both general and specific regulatory factors that function to accomplish negative and positive regulation of the INO1 promoter in response to inositol.

Indexed as

Repressor ProteinsSaccharomyces cerevisiae ProteinsAdenosine TriphosphatasesAllelesBase SequenceBasic Helix-Loop-Helix ProteinsChromosomal Proteins, Non-HistoneCloning, MolecularDNA-Binding ProteinsFungal ProteinsGene Expression Regulation, FungalInositolMolecular Sequence DataMyo-Inositol-1-Phosphate SynthaseNuclear ProteinsPromoter Regions, GeneticAdenosine TriphosphatasesBasic Helix-Loop-Helix ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsFungal ProteinsINO2 protein, S cerevisiaeINO4 protein, S cerevisiaeInositolMyo-Inositol-1-Phosphate SynthaseNuclear ProteinsRepressor ProteinsRNA, FungalRNA, MessengerSaccharomyces cerevisiae ProteinsSNF2 protein, S cerevisiaeSWI1 protein, S cerevisiaeSWI3 protein, S cerevisiaeTrans-ActivatorsTranscription Factors

Identifiers

PMID7753636
PMCPMC306872
OpenAlexW1986219286

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.