Evidence map›Paper›PMID 38489045›Full record

ArticleMolecular genetics and genomics : MGG2024

Deleterious variant in FAM71D cause male infertility with asthenoteratospermia.

Xiaobin Zhu, Liu Liu, Shixiong Tian, Guijun Zhao, Erlei Zhi, Qian Chen, Feng Zhang, Aijun Zhang, Shuyan Tang, Chunyu Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular genetics and genomics : MGG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Genetic etiological spectrum of sperm morphological abnormalities.Journal of assisted reproduction and genetics · 2024
    Review
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

10 authors at 2 institutions in 1 country.

Xiaobin Zhu *Department of Gynecology and Obstetrics, Reproductive Medical Center, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Liu Liu *Obstetrics and Gynecology Hospital, Institute of Medical Genetics and Genomics, Fudan University, Shanghai, 200011, China.
Shixiong Tian *Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, 200438, China.
Guijun ZhaoShanghai Institute of Medical Genetics, Shanghai Children's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200040, China.
Erlei ZhiUrologic Medical Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200940, China.
Qian ChenDepartment of Gynecology and Obstetrics, Reproductive Medical Center, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Feng ZhangInternational Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China.
Aijun ZhangDepartment of Gynecology and Obstetrics, Reproductive Medical Center, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. zhaj1268@163.com.
Shuyan TangObstetrics and Gynecology Hospital, Institute of Medical Genetics and Genomics, Fudan University, Shanghai, 200011, China. sy_tang05@outlook.com.
Chunyu LiuInternational Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China. 17111250002@fudan.edu.cn.ORCID http://orcid.org/0000-0002-6732-3758
Shanghai Jiao Tong University · CNFudan University · CN

Funding

China Postdoctoral Science Foundation 2020TQ0072National Key Research and Development Program of China 2021YFC2701400National Natural Science Foundation of China 31625015National Natural Science Foundation of China 32100480National Natural Science Foundation of China 32200485National Natural Science Foundation of China 82171586State Key Laboratory of Reproductive Medicine SKLRM-K202002
6 · The paper itself

Abstract

Asthenoteratospermia is a significant cause of male infertility. FAM71D (Family with sequence similarity 71, member D), as a novel protein exclusively expressed in the testis, has been found to be associated with sperm motility. However, the association of FAM71D mutation with male infertility has yet to be examined. Here, we conducted whole-exome sequencing and identified a homozygous missense mutation c.440G > A (p. Arg147Gln) of FAM71D in an asthenoteratospermia-affected man from a consanguineous family. The FAM71D variant is extremely rare in human population genome databases and predicted to be deleterious by multiple bioinformatics tools. Semen analysis indicated decreased sperm motility and obvious morphological abnormalities in sperm cells from the FAM71D-deficient man. Immunofluorescence assays revealed that the identified FAM71D mutation had an important influence on the assembly of sperm structure-related proteins. Furthermore, intra-cytoplasmic sperm injection (ICSI) treatment performed on the infertile man with FAM71D variant achieved a satisfactory outcome. Overall, our study identified FAM71D as a novel causative gene for male infertility with asthenoteratospermia, for which ICSI treatment may be suggested to acquire good prognosis. All these findings will provide effective guidance for genetic counselling and assisted reproduction treatments of asthenoteratospermia-affected subjects.

Indexed as

Infertility, MaleSemenHumansMaleMutationSpermatozoaSperm MotilityTestisAsthenoteratospermiaFAM71DICSIMale infertilityWhole-exome sequencing

Identifiers

PMID38489045
OpenAlexW4392872853

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.