Evidence map›Paper›PMID 22575490›Full record

ArticleDevelopmental biology2012

raw Functions through JNK signaling and cadherin-based adhesion to regulate Drosophila gonad morphogenesis.

Jennifer C Jemc, Alison B Milutinovich, Jill J Weyers, Yas Takeda, Mark Van Doren

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  7. Genetics · 2019
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  8. Degeneration of Injured Axons and Dendrites Requires Restraint of a Protective JNK Signaling Pathway by the Transmembrane Protein Raw.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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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

5 authors at 1 institution in 1 country.

Jennifer C JemcDepartment of Biology, Johns Hopkins University, 3400 N Charles St, Baltimore, MD 21218, USA.
Alison B Milutinovich
Jill J Weyers
Yas Takeda
Mark Van Doren
Johns Hopkins University · US

Funding

CELLULAR AND MOLECULAR BIOLOGYT32GM007231 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 1985 to 2020
$18.4M
Sexual development of the Drosophila gonadR01GM084356 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 2009 to 2016
$2.9M
Characterization of Factors Required for Gonad MorphogenesisF32GM085925 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI MIERISCH, JENNIFER COLLEEN JEMC · 2009 to 2010
$102k
NIGMS NIH HHS F32 GM085925NIGMS NIH HHS F32GM085925NIGMS NIH HHS R01 GM084356NIGMS NIH HHS R01GM084356NIGMS NIH HHS T32 GM007231
6 · The paper itself

Abstract

To form a gonad, germ cells (GCs) and somatic gonadal precursor cells (SGPs) must migrate to the correct location in the developing embryo and establish the cell-cell interactions necessary to create proper gonad architecture. During gonad morphogenesis, SGPs send out cellular extensions to ensheath the individual GCs and promote their development. We have identified mutations in the raw gene that result in a failure of the SGPs to ensheath the GCs, leading to defects in GC development. Using genetic analysis and gene expression studies, we find that Raw negatively regulates JNK signaling during gonad morphogenesis, and increased JNK signaling is sufficient to cause ensheathment defects. In particular, Raw functions upstream of the Drosophila Jun-related transcription factor to regulate its subcellular localization. Since JNK signaling regulates cell adhesion during the morphogenesis of many tissues, we examined the relationship between raw and the genes encoding Drosophila E-cadherin and β-catenin, which function together in cell adhesion. We find that loss of DE-cadherin strongly enhances the raw mutant gonad phenotype, while increasing DE-cadherin function rescues this phenotype. Further, loss of raw results in mislocalization of β-catenin away from the cell surface. Therefore, cadherin-based cell adhesion, likely at the level of β-catenin, is a primary mechanism by which Raw regulates germline-soma interaction.

Indexed as

MAP Kinase Signaling SystemAnimalsAnimals, Genetically ModifiedBase SequenceCadherinsCell AdhesionCytoskeletal ProteinsDNA PrimersDrosophilaDrosophila ProteinsGenes, InsectGerm CellsGonadsMutationCadherinsCytoskeletal ProteinsDNA PrimersDrosophila Proteinsraw protein, Drosophilashg protein, Drosophila

Identifiers

PMID22575490
PMCPMC3635074
OpenAlexW2122301470

What OpenQuestion holds

Textmetadata
LicenceTDM
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.