Evidence map›Paper›PMID 10713169›Full record

ArticleMolecular and cellular biology2000

Genetic analysis of the YDR1-BUR6 repressor complex reveals an intricate balance among transcriptional regulatory proteins in yeast.

S Kim, K Cabane, M Hampsey, D Reinberg

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. 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
1.5field-weighted citation impact, top 18% 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, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Regulation of TATA-binding protein dynamics in living yeast cells.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  5. Article
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  10. Direct stimulation of transcription by negative cofactor 2 (NC2) through TATA-binding protein (TBP).Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  11. Article
  12. Article
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  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

4 authors at 1 institution in 1 country.

S KimHoward Hughes Medical Institute, Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey 08854-5635, USA.
K Cabane
M Hampsey
D Reinberg
Howard Hughes Medical Institute · US

Funding

GENETIC ANALYSIS OF TRANSCRIPTION INITIATION IN YEASTR01GM039484 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HAMPSEY, MICHAEL · 1995 to 2012
$2.7M
REPRESSION AND REGULATION OF GENE EXPRESSIONR01GM048518 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI REINBERG, DANNY F · 1993 to 2000
$156k
GENETIC ANALYSIS OF TRANSLATION INITIATION IN YEASTR29GM039484 · NIGMS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI HAMPSEY, MICHAEL · 1988 to 1993
–
NIGMS NIH HHS GM39484NIGMS NIH HHS GM48518NIGMS NIH HHS R01 GM039484
6 · The paper itself

Abstract

A transcriptional repressor complex encoded by two essential genes, YDR1 and BUR6, was isolated from Saccharomyces cerevisiae and shown to be the functional counterpart of the human repressor complex Dr1-DRAP1. To elucidate the mechanism of repression by this complex, altered forms of Ydr1 and Bur6 were studied in vitro and in vivo. Deletion of the C-terminal 41 amino acids of Ydr1 resulted in loss of repressor activity and a growth defect, suggesting that the C-terminal domain of Ydr1 functions as a potent transcriptional repressor. A screen for extragenic suppressors of a cold-sensitive ydr1 (ydr1(cs)) mutant led to the identification of recessive mutations in the SIN4 gene, which encodes a component of the SRB-MED complex. The sin4 alleles suppressed not only ydr1(cs) mutations but also bur6(cs) mutations. In contrast, deletion of the gal11 gene, whose product is also a member of the SRB-MED complex, failed to suppress ydr1(cs) and bur6(cs) mutations, indicating that suppression is not due to general defects in the SRB-MED complex. Moreover, one of the sin4 alleles, but not the sin4 deletion, was found to specifically suppress the inviability of a ydr1 deletion, demonstrating that the essential function of Ydr1 becomes dispensable in a sin4 mutant background. Biochemical analysis of the SRB-MED complex from the sin4 suppressor strain revealed a structurally distinct form of the SRB-MED complex that lacks a subset of mediator subunits. These results define a delicate balance between positive and negative regulators of transcription operating through the Ydr1-Bur6 repressor complex.

Indexed as

Saccharomyces cerevisiae ProteinsAmino Acid SequenceATP-Binding Cassette TransportersFungal ProteinsGene Expression Regulation, FungalGenes, FungalGenotypeHumansMediator ComplexMolecular Sequence DataMutationPhosphoproteinsRepressor ProteinsSaccharomyces cerevisiaeSequence AlignmentTrans-ActivatorsATP-Binding Cassette TransportersBUR6 protein, S cerevisiaedown-regulator of transcription 1Fungal ProteinsGAL11 protein, S cerevisiaeMediator ComplexPDR5 protein, S cerevisiaePhosphoproteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsSIN4 protein, S cerevisiaeTrans-ActivatorsTranscription Factors

Identifiers

PMID10713169
PMCPMC85436
OpenAlexW2142086616

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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.