Evidence map›Paper›PMID 21966278›Full record

ArticlePLoS genetics2011

Novel interactions between actin and the proteasome revealed by complex haploinsufficiency.

Brian Haarer, Dimitra Aggeli, Susan Viggiano, Daniel J Burke, David C Amberg

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Actin dynamics in protein homeostasis.Bioscience reports · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Mapping a diversity of genetic interactions in yeast.Current opinion in systems biology · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Functional genomics in the study of yeast cell polarity: moving in the right direction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Review
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 at 2 institutions in 1 country.

Brian HaarerDepartment of Biochemistry and Molecular Biology, Upstate Medical University, State University of New York, Syracuse, New York, USA.
Dimitra Aggeli
Susan Viggiano
Daniel J Burke
David C Amberg
SUNY Upstate Medical University · USUniversity of Virginia Medical Center · US

Funding

Toward a Complete Genetic Description of the Yeast Actin CytoskeletonR01GM074992 · NIGMS · UPSTATE MEDICAL UNIVERSITY · PI AMBERG, DAVID C · 2007 to 2010
$1.5M
Mitotic regulation by checkpoints in budding yeastR01GM086502 · NIGMS · UNIVERSITY OF VIRGINIA · PI BURKE, DANIEL J · 2009 to 2012
$1.4M
NIGMS NIH HHS GM074992NIGMS NIH HHS GM86502NIGMS NIH HHS R01 GM074992NIGMS NIH HHS R01 GM086502
6 · The paper itself

Abstract

Saccharomyces cerevisiae has been a powerful model for uncovering the landscape of binary gene interactions through whole-genome screening. Complex heterozygous interactions are potentially important to human genetic disease as loss-of-function alleles are common in human genomes. We have been using complex haploinsufficiency (CHI) screening with the actin gene to identify genes related to actin function and as a model to determine the prevalence of CHI interactions in eukaryotic genomes. Previous CHI screening between actin and null alleles for non-essential genes uncovered ∼240 deleterious CHI interactions. In this report, we have extended CHI screening to null alleles for essential genes by mating a query strain to sporulations of heterozygous knock-out strains. Using an act1Δ query, knock-outs of 60 essential genes were found to be CHI with actin. Enriched in this collection were functional categories found in the previous screen against non-essential genes, including genes involved in cytoskeleton function and chaperone complexes that fold actin and tubulin. Novel to this screen was the identification of genes for components of the TFIID transcription complex and for the proteasome. We investigated a potential role for the proteasome in regulating the actin cytoskeleton and found that the proteasome physically associates with actin filaments in vitro and that some conditional mutations in proteasome genes have gross defects in actin organization. Whole-genome screening with actin as a query has confirmed that CHI interactions are important phenotypic drivers. Furthermore, CHI screening is another genetic tool to uncover novel functional connections. Here we report a previously unappreciated role for the proteasome in affecting actin organization and function.

Indexed as

ActinsAllelesCytoskeletonGenes, EssentialGenes, FungalHaploinsufficiencyHeterozygoteLeupeptinsMicrofilament ProteinsMutationPhenotypeProteasome Endopeptidase ComplexSaccharomyces cerevisiaeTranscription Factor TFIIDActinsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeLeupeptinsMicrofilament ProteinsProteasome Endopeptidase ComplexTranscription Factor TFIID

Identifiers

PMID21966278
PMCPMC3178594
OpenAlexW2118385485

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.