Evidence map›Paper›PMID 24552588›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

Notch signaling regulates ovarian follicle formation and coordinates follicular growth.

Dallas A Vanorny, Rexxi D Prasasya, Abha J Chalpe, Signe M Kilen, Kelly E Mayo

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
12.8field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.

  1. Roles of the Notch Signaling Pathway in Ovarian Functioning.Reproductive sciences (Thousand Oaks, Calif.) · 2021
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14 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

5 authors at 1 institution in 1 country.

Dallas A VanornyDepartment of Molecular Biosciences and Center for Reproductive Science, Northwestern University, Evanston, Illinois 60208.
Rexxi D Prasasya
Abha J Chalpe
Signe M Kilen
Kelly E Mayo
Northwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Transition Metal Regulation of Oocyte MaturationP01HD021921 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MAYO, KELLY E · 1987 to 2013
$18.5M
CELLULAR &MOLECULAR BASIS OF DISEASE TRAINING PROGRAMT32GM008061 · NIGMS · NORTHWESTERN UNIVERSITY · PI CARTHEW, RICHARD W. · 1985 to 2022
$17.1M
Physiology Core - Interdepartmental Two-photon Imaging CenterP30NS054850 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SURMEIER, DALTON JAMES · 2007 to 2012
$3.3M
NCI NIH HHS P30 CA060553NICHD NIH HHS P01 HD021921NIGMS NIH HHS T32 GM008061NIGMS NIH HHS T32 GM08061NINDS NIH HHS P30 NS054850
6 · The paper itself

Abstract

Ovarian follicles form through a process in which somatic pregranulosa cells encapsulate individual germ cells from germ cell syncytia. Complementary expression of the Notch ligand, Jagged1, in germ cells and the Notch receptor, Notch2, in pregranulosa cells suggests a role for Notch signaling in mediating cellular interactions during follicle assembly. Using a Notch reporter mouse, we demonstrate that Notch signaling is active within somatic cells of the embryonic ovary, and these cells undergo dramatic reorganization during follicle histogenesis. This coincides with a significant increase in the expression of the ligands, Jagged1 and Jagged2; the receptor, Notch2; and the target genes, Hes1 and Hey2. Histological examination of ovaries from mice with conditional deletion of Jagged1 within germ cells (J1 knockout [J1KO]) or Notch2 within granulosa cells (N2 knockout [N2KO]) reveals changes in follicle dynamics, including perturbations in the primordial follicle pool and antral follicle development. J1KO and N2KO ovaries also contain multi-oocytic follicles, which represent a failure to resolve germ cell syncytia, and follicles with enlarged oocytes but lacking somatic cell growth, signifying a potential role of Notch signaling in follicle activation and the coordination of follicle development. We also observed decreased cell proliferation and increased apoptosis in the somatic cells of both conditional knockout lines. As a consequence of these defects, J1KO female mice are subfertile; however, N2KO female mice remain fertile. This study demonstrates important functions for Jagged1 and Notch2 in the resolution of germ cell syncytia and the coordination of somatic and germ cell growth within follicles of the mouse ovary.

Indexed as

Signal TransductionAnimalsApoptosisCalcium-Binding ProteinsCell ProliferationFemaleGene DeletionGene Expression Regulation, DevelopmentalGenes, ReporterGerm CellsGranulosa CellsGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsJagged-1 ProteinMembrane ProteinsMiceCalcium-Binding Proteinsenhanced green fluorescent proteinGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsJag1 protein, mouseJagged-1 ProteinMembrane ProteinsNotch2 protein, mouseReceptor, Notch2Serrate-Jagged Proteins

Identifiers

PMID24552588
PMCPMC3968400
OpenAlexW1985375469

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.