Evidence map›Paper›PMID 9475737›Full record

ArticleGenetics1998

Genetic analysis of brahma: the Drosophila homolog of the yeast chromatin remodeling factor SWI2/SNF2.

L K Elfring, C Daniel, O Papoulas, R Deuring, M Sarte, S Moseley, S J Beek, W R Waldrip, G Daubresse, A DePace and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 192 citations in OpenAlex.

  1. Article
  2. Article
  3. ISWI catalyzes nucleosome sliding in condensed nucleosome arrays.Nature structural & molecular biology · 2024
    Article
  4. Article
  5. ISWI catalyzes nucleosome sliding in condensed nucleosome arrays.bioRxiv : the preprint server for biology · 2023
    Article
  6. Article
  7. Article
  8. Chromatin-Remodelling ATPasesInternational journal of molecular sciences · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

40 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 1 country.

L K ElfringDepartment of Biology, University of California, Santa Cruz 95064, USA.
C Daniel
O Papoulas
R Deuring
M Sarte
S Moseley
S J Beek
W R Waldrip
G Daubresse
A DePace
J A Kennison
J W Tamkun
University of California, Santa Cruz · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Studies of Chromatin Remodeling FactorsR01GM049883 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI TAMKUN, JOHN W. · 1993 to 2013
$3.9M
NIGMS NIH HHS GM49883
6 · The paper itself

Abstract

The Drosophila brahma (brm) gene encodes an activator of homeotic genes related to the yeast chromatin remodeling factor SWI2/SNF2. Here, we report the phenotype of null and dominant-negative brm mutations. Using mosaic analysis, we found that the complete loss of brm function decreases cell viability and causes defects in the peripheral nervous system of the adult. A dominant-negative brm mutation was generated by replacing a conserved lysine in the ATP-binding site of the BRM protein with an arginine. This mutation eliminates brm function in vivo but does not affect assembly of the 2-MD BRM complex. Expression of the dominant-negative BRM protein caused peripheral nervous system defects, homeotic transformations, and decreased viability. Consistent with these findings, the BRM protein is expressed at relatively high levels in nuclei throughout the developing organism. Site-directed mutagenesis was used to investigate the functions of conserved regions of the BRM protein. Domain II is essential for brm function and is required for the assembly or stability of the BRM complex. In spite of its conservation in numerous eukaryotic regulatory proteins, the deletion of the bromodomain of the BRM protein has no discernible phenotype.

Indexed as

Cell Cycle ProteinsNuclear ProteinsAmino Acid SequenceAnimalsConserved SequenceDNA-Binding ProteinsDrosophilaDrosophila ProteinsInsect ProteinsMolecular Sequence DataMutagenesis, Site-DirectedPhenotypeProtein Structure, TertiarySequence AlignmentSequence Homology, Amino AcidTrans-Activatorsbrm protein, DrosophilaCell Cycle ProteinsDNA-Binding ProteinsDrosophila ProteinsInsect ProteinsNuclear ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID9475737
PMCPMC1459776
OpenAlexW1895529587

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.