Evidence map›Paper›PMID 34473250›Full record

ArticleDevelopment (Cambridge, England)2021

Kpna6 deficiency causes infertility in male mice by disrupting spermatogenesis.

Na Liu, Fatimunnisa Qadri, Hauke Busch, Stefanie Huegel, Gabin Sihn, Ilya Chuykin, Enno Hartmann, Michael Bader, Franziska Rother

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. COPS5 is Essential for Sertoli Cell Function and Male Fertility in Mice.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Article
  5. Loss of the importiniScience · 2023
    Article
  6. SPAG17 mediates nuclear translocation of protamines during spermiogenesis.Frontiers in cell and developmental biology · 2023
    Article
  7. Analysis of Ser/Thr Kinase HASPIN-Interacting Proteins in the Spermatids.International journal of molecular sciences · 2022
    Article
  8. Article
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

9 authors at 2 institutions in 2 countries.

Na LiuMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.
Fatimunnisa QadriMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.
Hauke BuschMedical Systems Biology Division, Lübeck Institute of Experimental Dermatology and Institute for Cardiogenetics, University of Lübeck, Lübeck 23562, Germany.ORCID 0000-0003-4763-4521
Stefanie HuegelMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.
Gabin SihnMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.
Ilya ChuykinMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.ORCID 0000-0002-1773-6829
Enno HartmannInstitute for Biology, Center for Structural and Cellular Biology in Medicine, University of Lübeck, Lübeck 23562, Germany.
Michael BaderMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.
Franziska RotherMax Delbrück Center for Molecular Medicine, Berlin 13125, Germany.ORCID 0000-0002-4417-2192
Max Delbrück Center · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spermatogenesis is driven by an ordered series of events, which rely on trafficking of specific proteins between nucleus and cytoplasm. The karyopherin α family of proteins mediates movement of specific cargo proteins when bound to karyopherin β. Karyopherin α genes have distinct expression patterns in mouse testis, implying they may have unique roles during mammalian spermatogenesis. Here, we use a loss-of-function approach to determine specifically the role of Kpna6 in spermatogenesis and male fertility. We show that ablation of Kpna6 in male mice leads to infertility and has multiple cumulative effects on both germ cells and Sertoli cells. Kpna6-deficient mice exhibit impaired Sertoli cell function, including loss of Sertoli cells and a compromised nuclear localization of the androgen receptor. Furthermore, our data demonstrate devastating defects on spermiogenesis, including incomplete sperm maturation and a massive reduction in sperm number, accompanied by disturbed histone-protamine exchange, differential localization of the transcriptional regulator BRWD1 and altered expression of RFX2 target genes. Our work uncovers an essential role of Kpna6 in spermatogenesis and, hence, in male fertility.

Indexed as

SpermatogenesisActive Transport, Cell Nucleusalpha KaryopherinsAnimalsCell NucleusInfertility, MaleLoss of Function MutationMaleMiceMice, Inbred C57BLReceptors, AndrogenSertoli CellsSpermatogoniaalpha KaryopherinsKPNA6 protein, mouseReceptors, AndrogenImportinKaryopherinMale fertilityMouseSpermatogenesisTestis

Identifiers

PMID34473250
PMCPMC8513612
OpenAlexW3203284396

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.