Evidence map›Paper›PMID 35608054›Full record

ArticleDevelopment (Cambridge, England)2022

Loss of Prm1 leads to defective chromatin protamination, impaired PRM2 processing, reduced sperm motility and subfertility in male mice.

Gina Esther Merges, Julia Meier, Simon Schneider, Alexander Kruse, Andreas Christian Fröbius, Gregor Kirfel, Klaus Steger, Lena Arévalo, Hubert Schorle

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Meiotic prophase I disruption as a strategy for nonhormonal male contraception using small-molecule inhibitor JQ1.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Stability of epigenetic transgenerational inheritance of adult-onset disease and parturition abnormalities.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 3 institutions in 1 country.

Gina Esther MergesDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-5805-965X
Julia MeierDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.
Simon SchneiderDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-9894-5608
Alexander KruseDepartment of Urology, Pediatric Urology and Andrology, Section Molecular Andrology, Biomedical Research Center of the Justus-Liebig University, 35392 Giessen, Germany.ORCID 0000-0001-5526-9347
Andreas Christian FröbiusDepartment of Urology, Pediatric Urology and Andrology, Section Molecular Andrology, Biomedical Research Center of the Justus-Liebig University, 35392 Giessen, Germany.ORCID 0000-0002-0343-6067
Gregor KirfelDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, 53121 Bonn, Germany.
Klaus StegerDepartment of Urology, Pediatric Urology and Andrology, Section Molecular Andrology, Biomedical Research Center of the Justus-Liebig University, 35392 Giessen, Germany.ORCID 0000-0002-2104-0840
Lena ArévaloDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-0681-0392
Hubert SchorleDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-8272-0076
University Hospital Bonn · DEJustus-Liebig-Universität Gießen · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the key events during spermiogenesis is the hypercondensation of chromatin by substitution of the majority of histones by protamines. In humans and mice, protamine 1 (PRM1/Prm1) and protamine 2 (PRM2/Prm2) are expressed in a species-specific ratio. Using CRISPR-Cas9-mediated gene editing, we generated Prm1-deficient mice and demonstrated that Prm1+/- mice were subfertile, whereas Prm1-/- mice were infertile. Prm1-/- and Prm2-/- sperm showed high levels of reactive oxygen species-mediated DNA damage and increased histone retention. In contrast, Prm1+/- sperm displayed only moderate DNA damage. The majority of Prm1+/- sperm were CMA3 positive, indicating protamine-deficient chromatin, although this was not the result of increased histone retention in Prm1+/- sperm. However, sperm from Prm1+/- and Prm1-/- mice contained high levels of incompletely processed PRM2. Furthermore, the PRM1:PRM2 ratio was skewed from 1:2 in wild type to 1:5 in Prm1+/- animals. Our results reveal that PRM1 is required for proper PRM2 processing to produce mature PRM2, which, together with PRM1, is able to hypercondense DNA. Thus, the species-specific PRM1:PRM2 ratio has to be precisely controlled in order to retain full fertility.

Indexed as

AsthenozoospermiaInfertility, MaleAnimalsChromatinHistonesMaleMiceProtaminesSpermatozoaSperm MotilityChromatinHistonesPrm1 protein, mouseProtaminesChromatin condensationInfertilityMousePRM2 processingProtamine 1 (Prm1)Protamine ratioSubfertility

Identifiers

PMID35608054
PMCPMC9270976
OpenAlexW4281931231

What OpenQuestion holds

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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.