Evidence map›Paper›PMID 27814383›Full record

ArticlePloS one2016

Adult Gli2+/-;Gli3Δ699/+ Male and Female Mice Display a Spectrum of Genital Malformation.

Fei He, Pedram Akbari, Rong Mo, Jennifer J Zhang, Chi-Chung Hui, Peter C Kim, Walid A Farhat

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  5. Streamlined identification of clinically and functionally relevant genetic regulators of lower-tract urogenital development.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 4 institutions in 2 countries.

Fei HeProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Pedram AkbariProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Rong MoProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Jennifer J ZhangProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Chi-Chung HuiProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Peter C KimSheikh Zayed Institute for Pediatric Surgical Innovation, Children's National Health System, Washington, DC, United States of America.
Walid A FarhatProgram in Developmental & Stem Cell Biology, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada.
Hospital for Sick Children · CAChildren's National · USSickKids Foundation · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disorders of sexual development (DSD) encompass a broad spectrum of urogenital malformations and are amongst the most common congenital birth defects. Although key genetic factors such as the hedgehog (Hh) family have been identified, a unifying postnatally viable model displaying the spectrum of male and female urogenital malformations has not yet been reported. Since human cases are diagnosed and treated at various stages postnatally, equivalent mouse models enabling analysis at similar stages are of significant interest. Additionally, all non-Hh based genetic models investigating DSD display normal females, leaving female urogenital development largely unknown. Here, we generated compound mutant mice, Gli2+/-;Gli3Δ699/+, which exhibit a spectrum of urogenital malformations in both males and females upon birth, and also carried them well into adulthood. Analysis of embryonic day (E)18.5 and adult mice revealed shortened anogenital distance (AGD), open ventral urethral groove, incomplete fusion of scrotal sac, abnormal penile size and structure, and incomplete testicular descent with hypoplasia in male mice, whereas female mutant mice displayed reduced AGD, urinary incontinence, and a number of uterine anomalies such as vaginal duplication. Male and female fertility was also investigated via breeding cages, and it was identified that male mice were infertile while females were unable to deliver despite becoming impregnated. We propose that Gli2+/-;Gli3Δ699/+ mice can serve as a genetic mouse model for common DSD such as cryptorchidism, hypospadias, and incomplete fusion of the scrotal sac in males, and a spectrum of uterine and vaginal abnormalities along with urinary incontinence in females, which could prove essential in revealing new insights into their equivalent diseases in humans.

Indexed as

Anal CanalAnimalsCryptorchidismDisease Models, AnimalFemaleHypospadiasKruppel-Like Transcription FactorsMaleMiceNerve Tissue ProteinsPenisUrogenital AbnormalitiesUterusVaginaZinc Finger Protein Gli2Zinc Finger Protein Gli3Gli2 protein, mouseGli3 protein, mouseKruppel-Like Transcription FactorsNerve Tissue ProteinsZinc Finger Protein Gli2Zinc Finger Protein Gli3

Identifiers

PMID27814383
PMCPMC5096680
OpenAlexW2546727772

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.