Evidence map›Paper›PMID 37800308›Full record

ArticleDevelopment (Cambridge, England)2023

Actl7b deficiency leads to mislocalization of LC8 type dynein light chains and disruption of murine spermatogenesis.

Gina E Merges, Lena Arévalo, Andjela Kovacevic, Keerthika Lohanadan, Dirk G de Rooij, Carla Simon, Melanie Jokwitz, Walter Witke, Hubert Schorle

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.0field-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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. 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 3 institutions in 2 countries.

Gina E MergesDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-5805-965X
Lena ArévaloDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0002-0681-0392
Andjela KovacevicDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-7719-2467
Keerthika LohanadanDepartment of Molecular Cell Biology, Institute for Cell Biology, University of Bonn, 53121 Bonn, Germany.
Dirk G de RooijReproductive Biology Group, Division of Developmental Biology, Department of Biology, Faculty of Science, Utrecht University, 3584 CH Utrecht, The Netherlands.ORCID 0000-0003-3932-4419
Carla SimonCell Migration Unit, Institute of Genetics, University of Bonn, 53115 Bonn, Germany.ORCID 0009-0009-9687-3730
Melanie JokwitzCell Migration Unit, Institute of Genetics, University of Bonn, 53115 Bonn, Germany.
Walter WitkeCell Migration Unit, Institute of Genetics, University of Bonn, 53115 Bonn, Germany.ORCID 0000-0001-5018-0060
Hubert SchorleDepartment of Developmental Pathology, Institute of Pathology, University Hospital Bonn, 53127 Bonn, Germany.ORCID 0000-0001-8272-0076
University Hospital Bonn · DEUniversity of Bonn · DEUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Actin-related proteins (Arps) are classified according to their similarity to actin and are involved in diverse cellular processes. ACTL7B is a testis-specific Arp, and is highly conserved in rodents and primates. ACTL7B is specifically expressed in round and elongating spermatids during spermiogenesis. Here, we have generated an Actl7b-null allele in mice to unravel the role of ACTL7B in sperm formation. Male mice homozygous for the Actl7b-null allele (Actl7b-/-) were infertile, whereas heterozygous males (Actl7b+/-) were fertile. Severe spermatid defects, such as detached acrosomes, disrupted membranes and flagella malformations start to appear after spermiogenesis step 9 in Actl7b-/- mice, finally resulting in spermatogenic arrest. Abnormal spermatids were degraded and levels of autophagy markers were increased. Co-immunoprecipitation with mass spectrometry experiments identified an interaction between ACTL7B and the LC8 dynein light chains DYNLL1 and DYNLL2, which are first detected in step 9 spermatids and mislocalized when ACTL7B is absent. Our data unequivocally establish that mutations in ACTL7B are directly related to male infertility, pressing for additional research in humans.

Indexed as

ActinsDyneinsAnimalsCytoplasmic DyneinsHumansMaleMiceSemenSpermatidsSpermatogenesisSpermatozoaTestisActinsActl7b protein, mouseCytoplasmic DyneinsDyneinsDYNLL1 protein, mouseActin-related proteinsActl7bInfertilityLC8 light chainsMouseSpermatogenesis

Identifiers

PMID37800308
PMCPMC10652042
OpenAlexW4387392712

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.