Evidence map›Paper›PMID 22069496›Full record

ArticlePloS one2011

Mll5 is required for normal spermatogenesis.

Damian B Yap, David C Walker, Leah M Prentice, Steven McKinney, Gulisa Turashvili, Katrin Mooslehner-Allen, Teresa Ruiz de Algara, John Fee, Xavier d'Anglemont de Tassigny, William H Colledge and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  5. Case Report:Frontiers in pediatrics · 2021
    Article
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. MLL5 (KMT2E): structure, function, and clinical relevance.Cellular and molecular life sciences : CMLS · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

11 authors at 3 institutions in 2 countries.

Damian B YapDepartment of Molecular Oncology, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada.
David C Walker
Leah M Prentice
Steven McKinney
Gulisa Turashvili
Katrin Mooslehner-Allen
Teresa Ruiz de Algara
John Fee
Xavier d'Anglemont de Tassigny
William H Colledge
Samuel Aparicio
University of British Columbia · CAUniversity of Cambridge · GBAddenbrooke's Hospital · GB

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

backgroundMll5 is currently a member of the Mll family of SET domain histone methyltransferase proteins but studies have also showed that it could be part of the SET3 branch of proteins. Recently, constitutive knock out animal studies have shown that Mll5 is required for proper haematopoietic stem cell differentiation, and loss of Mll5 results in synthetic lethality for genome de-methylation. Mll5 deficient male mice are infertile and here we analyse the consequences of Mll5 deficiency for spermatogenesis. METHODOLOGY/PRINCIPAL

findingsMll5 deficient male mice, but not female mice, are infertile. Here we show using RNA in-situ hybridization that Mll5 is expressed in the germ cells of the testes of wild type mice. Consistent with the expression of Mll5, we demonstrate by electron microscopy, video microscopy and in vitro fertilisation techniques that Mll5 deficient mice have defects in terminal maturation and packaging of sperm. The defects seen include detachment of the acrosomal cap and impaired excess cytoplasm removal. Functional tests of sperm motility show a lack of progressive motility of spermatozoa from Mll5 deficient animals. None of these defects could be rescued by in vitro fertilization. Using microarray analysis we show that transcripts implicated in spermatogenesis are dysregulated. CONCLUSIONS/SIGNIFICANCE: Our data demonstrate a clear role of Mll5 in mammalian spermatogenesis at the level of terminal differentiation providing further support for its classification in the SET3 branch of proteins. Moreover, this study identifies Tlk2, Utx, Gpr64, Sult4a1, Rap2ip, Vstm2 and HoxA10 as possible Mll5 targets that together may account for the observed spermatozoa maturation defects.

Indexed as

AnimalsBiomarkersFemaleGene Expression ProfilingHistone-Lysine N-MethyltransferaseHomozygoteHumansInfertility, MaleMaleMiceMice, TransgenicMicroscopy, ElectronMicroscopy, VideoOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionRNA, MessengerBiomarkersHistone-Lysine N-MethyltransferaseMLL5 protein, mouseRNA, Messenger

Identifiers

PMID22069496
PMCPMC3206077
OpenAlexW2072337271

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.