Evidence map›Paper›PMID 41871121›Full record

ArticlePLoS genetics2026

Genetic and functional characterization of AMH Signaling in Zebrafish - Evidence for Roles of Amh-Bmpr2a-Bmpr1bb Pathway in Controlling Gonadal Homeostasis.

Yiming Yue, Chu Zeng, Xin Zhang, Chao Bian, Zhiwei Zhang, Kun Wu, Weiting Chen, Xianqing Zhou, Ling Lu, Nana Ai and 1 more

Abstract read
In one paragraph

Article in PLoS genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yiming YueDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Chu ZengDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Xin ZhangDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.ORCID https://orcid.org/0000-0001-6631-6145
Chao BianLaboratory of Aquatic Genomics, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China.
Zhiwei ZhangDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Kun WuDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Weiting ChenDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Xianqing ZhouDepartment of Toxicology and Hygienic Chemistry, School of Public Health, Capital Medical University, Beijing, China.
Ling LuKey Laboratory of Marine Drugs, The Ministry of Education of China, School of Medicine and Pharmacy, Ocean University of China, Qingdao, China.
Nana AiDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.
Wei GeDepartment of Biomedical Sciences and Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Macau, China.ORCID https://orcid.org/0000-0002-4296-1585

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-Müllerian hormone (AMH), a member of the TGF-β superfamily, plays a crucial role in Müllerian duct regression in mammals. AMH signals through a specific type II receptor (AMHRII) and a type I receptor to activate the downstream Smad1/5/9 signaling pathway. Interestingly, non-mammalian vertebrates, including teleosts, also express AMH despite lacking Müllerian ducts. Accumulating evidence indicates that AMH influences gonadal development and function across vertebrates. Intriguingly, zebrafish, a popular model organism, possesses AMH (Amh/amh) but lacks specific type II receptor (Amhr2). Based on our previous studies and data from others, we propose that Amh may signal through a novel pathway in zebrafish involving the BMP type II receptor Bmpr2a and type I receptor Bmpr1bb. In this study, we provide genetic and functional evidence for the existence of the Amh-Bmpr2a-Bmpr1bb signaling pathway in zebrafish and its role in controlling gonadal homeostasis. Our experimental data excluded the participation of Bmpr2b and Bmpr1ba, paralogues of Bmpr2a and Bmpr1bb respectively, in Amh signaling. Additionally, we also provide genetic evidence that the phenotypes exhibited by amh, bmpr2a, and bmpr1bb mutants, e.g., gonadal hypertrophy, were all dependent on gonadotropin signaling, and that the two gonadotropins (FSH and LH) could both drive the development of hypertrophic gonadal growth resulting from dysfunction in the Amh-Bmpr2a-Bmpr1bb signaling pathway, with FSH showing a more immediate effect in females. In summary, the present study provides comprehensive evidence for Amh signaling through Bmpr2a-Bmpr1bb pathway and its interplay with gonadotropins in controlling germ cell proliferation and differentiation, thereby maintaining gonadal homeostasis.

Indexed as

Anti-Mullerian HormoneBone Morphogenetic Protein Receptors, Type IBone Morphogenetic Protein Receptors, Type IIGonadsZebrafishZebrafish ProteinsAnimalsFemaleGene Expression Regulation, DevelopmentalHomeostasisMaleMullerian DuctsReceptors, PeptideSignal TransductionAnti-Mullerian HormoneBone Morphogenetic Protein Receptors, Type IBone Morphogenetic Protein Receptors, Type IIReceptors, PeptideZebrafish Proteins

Identifiers

PMID41871121
PMCPMC13095126

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.