Evidence map›Paper›PMID 22649080›Full record

ArticleGenetics2012

Bypassing the Greatwall-Endosulfine pathway: plasticity of a pivotal cell-cycle regulatory module in Drosophila melanogaster and Caenorhabditis elegans.

Min-Young Kim, Elisabetta Bucciarelli, Diane G Morton, Byron C Williams, Kristina Blake-Hodek, Claudia Pellacani, Jessica R Von Stetina, Xiaoqian Hu, Maria Patrizia Somma, Daniela Drummond-Barbosa and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Greatwall-Endos-PP2A/B55Open biology · 2024
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  9. MPF-based meiotic cell cycle control: Half a century of lessons from starfish oocytes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2018
    Review
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  13. Review
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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

11 authors at 4 institutions in 2 countries.

Min-Young KimDepartment of Biochemistry and Molecular Biology, Division of Reproductive Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Elisabetta Bucciarelli
Diane G Morton
Byron C Williams
Kristina Blake-Hodek
Claudia Pellacani
Jessica R Von Stetina
Xiaoqian Hu
Maria Patrizia Somma
Daniela Drummond-Barbosa
Michael L Goldberg
Cornell University · USInstitute of Molecular Biology and Pathology · ITJohns Hopkins University · USVanderbilt University Medical Center · US

Funding

Greatwall Kinase and the Mitotic Control of Phosphatase ActivityR01GM048430 · NIGMS · CORNELL UNIVERSITY ITHACA · PI GOLDBERG, MICHAEL L · 1992 to 2017
$6.6M
Nutrient Sensing in Adipocytes and the Control of Oogenesis in DrosophilaR01GM069875 · NIGMS · VANDERBILT UNIVERSITY · PI DRUMMOND-BARBOSA, DANIELA · 2005 to 2020
$5.2M
NIGMS NIH HHS R01 GM048430NIGMS NIH HHS R01 GM069875
6 · The paper itself

Abstract

In vertebrates, mitotic and meiotic M phase is facilitated by the kinase Greatwall (Gwl), which phosphorylates a conserved sequence in the effector Endosulfine (Endos). Phosphorylated Endos inactivates the phosphatase PP2A/B55 to stabilize M-phase-specific phosphorylations added to many proteins by cyclin-dependent kinases (CDKs). We show here that this module functions essentially identically in Drosophila melanogaster and is necessary for proper mitotic and meiotic cell division in a wide variety of tissues. Despite the importance and evolutionary conservation of this pathway between insects and vertebrates, it can be bypassed in at least two situations. First, heterozygosity for loss-of-function mutations of twins, which encodes the Drosophila B55 protein, suppresses the effects of endos or gwl mutations. Several types of cell division occur normally in twins heterozygotes in the complete absence of Endos or the near absence of Gwl. Second, this module is nonessential in the nematode Caenorhaditis elegans. The worm genome does not contain an obvious ortholog of gwl, although it encodes a single Endos protein with a surprisingly well-conserved Gwl target site. Deletion of this site from worm Endos has no obvious effects on cell divisions involved in viability or reproduction under normal laboratory conditions. In contrast to these situations, removal of one copy of twins does not completely bypass the requirement for endos or gwl for Drosophila female fertility, although reducing twins dosage reverses the meiotic maturation defects of hypomorphic gwl mutants. These results have interesting implications for the function and evolution of the mechanisms modulating removal of CDK-directed phosphorylations.

Indexed as

Signal TransductionAllelesAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCarboxylic Ester HydrolasesCell CycleDrosophila melanogasterDrosophila ProteinsFemaleGene DeletionGene OrderHeterozygoteIntercellular Signaling Peptides and ProteinsMaleMeiosisCarboxylic Ester HydrolasesDrosophila ProteinsendosulfineGwl protein, DrosophilaIntercellular Signaling Peptides and ProteinsPeptidesPhosphoprotein Phosphatasesprotein phosphatase methylesterase-1Protein Serine-Threonine KinasesProtein Subunits

Identifiers

PMID22649080
PMCPMC3416000
OpenAlexW1966294190

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.