Evidence map›Paper›PMID 27833122›Full record

ArticleScientific reports2016

Re-visiting the Protamine-2 locus: deletion, but not haploinsufficiency, renders male mice infertile.

Simon Schneider, Melanie Balbach, Jan F Jikeli, Daniela Fietz, Daniel Nettersheim, Sina Jostes, Rovenna Schmidt, Monika Kressin, Martin Bergmann, Dagmar Wachten and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 79 citations in OpenAlex.

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  6. Protamine lacunae preserve the paternal chromatin landscape in sperm.bioRxiv : the preprint server for biology · 2025
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  13. Review
  14. Protamine 2 deficiency results in Septin 12 abnormalities.Frontiers in cell and developmental biology · 2024
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  15. Article
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  19. iScience · 2023
    Article
  20. SPAG17 mediates nuclear translocation of protamines during spermiogenesis.Frontiers in cell and developmental biology · 2023
    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

12 authors at 3 institutions in 1 country.

Simon SchneiderInstitute of Pathology, Department of Developmental Pathology, University of Bonn Medical School, Bonn, Germany.
Melanie BalbachMinerva Max Planck Research Group - Molecular Physiology, Center of Advanced European Studies and Research, Bonn, Germany.
Jan F JikeliMinerva Max Planck Research Group - Molecular Physiology, Center of Advanced European Studies and Research, Bonn, Germany.
Daniela FietzInstitute of Veterinary-Anatomy, -Histology and -Embryology, Justus-Liebig University, Giessen, Germany.
Daniel NettersheimInstitute of Pathology, Department of Developmental Pathology, University of Bonn Medical School, Bonn, Germany.
Sina JostesInstitute of Pathology, Department of Developmental Pathology, University of Bonn Medical School, Bonn, Germany.
Rovenna SchmidtInstitute of Veterinary-Anatomy, -Histology and -Embryology, Justus-Liebig University, Giessen, Germany.
Monika KressinInstitute of Veterinary-Anatomy, -Histology and -Embryology, Justus-Liebig University, Giessen, Germany.
Martin BergmannInstitute of Veterinary-Anatomy, -Histology and -Embryology, Justus-Liebig University, Giessen, Germany.
Dagmar WachtenMinerva Max Planck Research Group - Molecular Physiology, Center of Advanced European Studies and Research, Bonn, Germany.
Klaus StegerDepartment of Urology, Pediatric Urology and Andrology, Section Molecular Andrology, Biomedical Research Center of the Justus-Liebig University, Giessen, Germany.
Hubert SchorleInstitute of Pathology, Department of Developmental Pathology, University of Bonn Medical School, Bonn, Germany.
University of Giessen · DEUniversity of Bonn · DECenter of Advanced European Studies and Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protamines are arginine-rich DNA-binding proteins that replace histones in elongating spermatids. This leads to hypercondensation of chromatin and ensures physiological sperm morphology, thereby protecting DNA integrity. In mice and humans, two protamines, protamine-1 (Prm1) and protamine-2 (Prm2) are expressed in a species-specific ratio. In humans, alterations of this PRM1/PRM2 ratio is associated with subfertility. By applying CRISPR/Cas9 mediated gene-editing in oocytes, we established Prm2-deficient mice. Surprisingly, heterozygous males remained fertile with sperm displaying normal head morphology and motility. In Prm2-deficient sperm, however, DNA-hypercondensation and acrosome formation was severely impaired. Further, the sperm displayed severe membrane defects resulting in immotility. Thus, lack of Prm2 leads not only to impaired histone to protamine exchange and disturbed DNA-hypercondensation, but also to severe membrane defects resulting in immotility. Interestingly, previous attempts using a regular gene-targeting approach failed to establish Prm2-deficient mice. This was due to the fact that already chimeric animals generated with Prm2

Indexed as

AnimalsBase SequenceCRISPR-Cas SystemsExonsFemaleGenetic Association StudiesGenetic LociHaploinsufficiencyHistonesInfertility, MaleMaleMiceProtaminesSequence DeletionSpermatogenesisSpermatozoaHistonesPrm1 protein, mouseprotamine 2Protamines

Identifiers

PMID27833122
PMCPMC5105070
OpenAlexW2555779600

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.