Evidence map›Paper›PMID 31301298›Full record

ReviewDevelopmental biology2019

AMH and AMHR2 mutations: A spectrum of reproductive phenotypes across vertebrate species.

Rachel D Mullen, Alejandra E Ontiveros, Malcolm M Moses, Richard R Behringer

Open access · greenAbstract readReview
In one paragraph

Review in Developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
3.6field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Rachel D MullenDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Alejandra E OntiverosDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, 77030, USA.
Malcolm M MosesDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Program in Genetics and Epigenetics, MD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences, Houston, TX, 77030, USA.
Richard R BehringerDepartment of Genetics, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA; Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, 77030, USA; Program in Genetics and Epigenetics, MD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences, Houston, TX, 77030, USA. Electronic address: rrb@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
Molecular Genetics of Female Reproductive TractR01HD030284 · NICHD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BEHRINGER, RICHARD R · 1994 to 2013
$4.5M
Female Reproductive Tract Development in the MouseR37HD030284 · NICHD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BEHRINGER, RICHARD R · 2014 to 2023
$4.2M
NICHD NIH HHS R01 HD030284NICHD NIH HHS R37 HD030284NIGMS NIH HHS R25 GM056929
6 · The paper itself

Abstract

Anti-Müllerian hormone (AMH) is a member of the Transforming Growth Factor-β family of secreted signaling proteins. AMH is expressed in Sertoli cells of the fetal and adult testes and granulosa cells of the postnatal ovary. AMH is required for the regression of the Müllerian ducts in mammalian fetuses during male differentiation. AMH signals through its Type II receptor, AMHR2. AMHR2 is expressed in mesenchyme adjacent to the Müllerian ducts, and in Sertoli, Leydig, and granulosa cells. Although AMH and AMHR2 genes have been identified in numerous vertebrate species, spontaneous or engineered mutations or variants have been found or created in only a few mammals and teleost fishes. AMH or AMHR2 mutations in mammals lead to the development of Persistent Müllerian Duct Syndrome (PMDS), a recessive condition in which affected males are fully virilized but retain Müllerian duct-derived tissues, including a uterus and oviducts, and in human and dog, undescended testes. Amh mutant female mice had accelerated ovarian primordial follicle recruitment, suggesting a role for AMH in regulating germ cells. amh and amhr2 mutations have also been experimentally generated in various teleost fishes. Depending on the fish species, loss of AMH signaling results in infertility, germ cell tumors, or male-to-female sex reversal. Here we compare the spectrum of phenotypes caused by AMH and AMHR2 mutations in a variety of vertebrate species. There are both common and unique phenotypes between species, highlighting the range of biological processes regulated by AMH signaling.

Indexed as

MutationAnimalsAnti-Mullerian HormoneDisorder of Sex Development, 46,XYFemaleHumansMalePhenotypeReceptors, PeptideReceptors, Transforming Growth Factor betaReproductionSpecies SpecificityVertebratesAnti-Mullerian Hormoneanti-Mullerian hormone receptorReceptors, PeptideReceptors, Transforming Growth Factor betaFertilityGametogenesisMüllerian duct regressionSex determinationTesticular descent

Identifiers

PMID31301298
PMCPMC6754765
OpenAlexW2957348823

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.