Evidence map›Paper›PMID 38570187›Full record

ArticleLife science alliance2024

Genetic mutation of

Brendan J Houston, D Jo Merriner, G Gemma Stathatos, Joseph H Nguyen, Anne E O'Connor, Alexandra M Lopes, Donald F Conrad, Mark Baker, Jessica Em Dunleavy, Moira K O'Bryan

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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

10 authors at 4 institutions in 3 countries.

Brendan J HoustonSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia brendan.houston@unimelb.edu.au.ORCID 0000-0002-1078-756X
D Jo MerrinerSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.
G Gemma StathatosSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.
Joseph H NguyenSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.
Anne E O'ConnorSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.
Alexandra M LopesInstituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Donald F ConradOregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR, USA.
Mark BakerSchool of Environmental and Life Sciences, The University of Newcastle, Callaghan, Australia.
Jessica Em DunleavySchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.
Moira K O'BryanSchool of BioSciences and Bio21 Molecular Sciences and Biotechnology Institute, The University of Melbourne, Parkville, Australia.ORCID 0000-0001-7298-4940
Biotechnology Institute · USOregon National Primate Research Center · USUniversidade do Porto · PTUniversity of Newcastle Australia · AU

Funding

GENOMICS OF SPERMATOGENIC IMPAIRMENTR01HD078641 · NICHD · WASHINGTON UNIVERSITY · PI Kenneth Ivan Aston, DONALD F. CONRAD · 2014 to 2026
$6.3M
NICHD NIH HHS R01 HD078641
6 · The paper itself

Abstract

The transition zone is a specialised gate at the base of cilia/flagella, which separates the ciliary compartment from the cytoplasm and strictly regulates protein entry. We identified a potential new regulator of the male germ cell transition zone, CEP76. We demonstrated that CEP76 was involved in the selective entry and incorporation of key proteins required for sperm function and fertility into the ciliary compartment and ultimately the sperm tail. In the mutant, sperm tails were shorter and immotile as a consequence of deficits in essential sperm motility proteins including DNAH2 and AKAP4, which accumulated at the sperm neck in the mutant. Severe annulus, fibrous sheath, and outer dense fibre abnormalities were also detected in sperm lacking CEP76. Finally, we identified that CEP76 dictates annulus positioning and structure. This study suggests CEP76 as a male germ cell transition zone protein and adds further evidence to the hypothesis that the spermatid transition zone and annulus are part of the same functional structure.

Indexed as

Infertility, MaleSperm TailHumansMaleMutationSemenSperm Motility

Identifiers

PMID38570187
PMCPMC10992998
OpenAlexW4393862656

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.