Evidence map›Paper›PMID 23209443›Full record

ArticlePLoS genetics2012

Deubiquitylation machinery is required for embryonic polarity in Caenorhabditis elegans.

Richard J McCloskey, Kenneth J Kemphues

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. 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
1.0field-weighted citation impact, top 30% 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, 22 citations in OpenAlex.

  1. Article
  2. USP7 regulates ALS-associated proteotoxicity and quality control through the NEDD4L-SMAD pathway.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  3. Going with the flow: insights fromPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Principles of PAR polarity in Caenorhabditis elegans embryos.Nature reviews. Molecular cell biology · 2013
    Review
  12. The PAR network: redundancy and robustness in a symmetry-breaking system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Review
  13. Article
  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

2 authors at 1 institution in 1 country.

Richard J McCloskeyDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York, United States of America.
Kenneth J Kemphues
Cornell University · US

Funding

PREDOCTORAL TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM007273 · NIGMS · CORNELL UNIVERSITY ITHACA · PI BRETSCHER, ANTHONY P. · 1985 to 2019
$11.6M
Asymmetric Cell Division in C. Elegans EmbryosR01GM079112 · NIGMS · CORNELL UNIVERSITY · PI KEMPHUES, KENNETH J. · 2006 to 2014
$3.1M
NIGMS NIH HHS NIH R01 GM079112NIGMS NIH HHS R01 GM079112NIGMS NIH HHS T32 GM007273NIGMS NIH HHS T32GM007273
6 · The paper itself

Abstract

The Caenorhabditis elegans one-cell embryo polarizes in response to a cue from the paternally donated centrosome and asymmetrically segregates cell fate determinants that direct the developmental program of the worm. We have found that genes encoding putative deubiquitylating enzymes (DUBs) are required for polarization of one-cell embryos. Maternal loss of the proteins MATH-33 and USP-47 leads to variable inability to correctly establish and maintain asymmetry as defined by posterior and anterior polarity proteins PAR-2 and PAR-3. The first observable defect is variable positioning of the centrosome with respect to the cell cortex and the male pronucleus. The severity of the polarity defects correlates with distance of the centrosome from the cortex. Furthermore, polarity defects can be bypassed by mutations that bring the centrosome in close proximity to the cortex. In addition we find that polarity and centrosome positioning defects can be suppressed by compromising protein turnover. We propose that the DUB activity of MATH-33 and USP-47 stabilizes one or more proteins required for association of the centrosome with the cortex. Because these DUBs are homologous to two members of a group of DUBs that act in fission yeast polarity, we tested additional members of that family and found that another C. elegans DUB gene, usp-46, also contributes to polarity. Our finding that deubiquitylating enzymes required for polarity in Schizosaccharomyces pombe are also required in C. elegans raises the possibility that these DUBs act through an evolutionarily conserved mechanism to control cell polarity.

Indexed as

Cell PolarityEmbryonic DevelopmentUbiquitinationAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DifferentiationCentrosomeCytoplasmEmbryo, NonmammalianEndopeptidasesMaleMutationProtein Serine-Threonine KinasesUbiquitin-Specific ProteasesCaenorhabditis elegans ProteinsEndopeptidasesMATH-33 protein, C eleganspar-2 protein, C elegansPAR-3 protein, C elegansProtein Serine-Threonine KinasesT05H10.1 protein, C elegansUbiquitin-Specific Proteases

Identifiers

PMID23209443
PMCPMC3510043
OpenAlexW2034203346

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.