Evidence map›Paper›PMID 23884444›Full record

ArticleDevelopment (Cambridge, England)2013

The polyubiquitin gene Ubi-p63E is essential for male meiotic cell cycle progression and germ cell differentiation in Drosophila.

Chenggang Lu, Jongmin Kim, Margaret T Fuller

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Comparative Ubiquitome Analysis Reveals Deubiquitinating Effects Induced byInternational journal of molecular sciences · 2022
    Article
  4. Article
  5. Article
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  8. Review
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  10. Article
  11. Article
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  13. Article
  14. USP5 Is Dispensable for Monoubiquitin Maintenance in Drosophila.The Journal of biological chemistry · 2016
    Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Chenggang LuDepartment of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305-5329, USA.
Jongmin Kim
Margaret T Fuller
Stanford University · US

Funding

Regulation of Spermatocyte Transcription by Testis TAFSR01GM061986 · NIGMS · STANFORD UNIVERSITY · PI FULLER, MARGARET T · 2000 to 2017
$5.1M
NIGMS NIH HHS 3 R01 GM061986NIGMS NIH HHS R01 GM061986
6 · The paper itself

Abstract

The ubiquitin proteasome system (UPS) regulates many biological pathways by post-translationally ubiquitylating proteins for degradation. Although maintaining a dynamic balance between free ubiquitin and ubiquitylated proteins is key to UPS function, the mechanisms that regulate ubiquitin homeostasis in different tissues through development are not clear. Here we show, via analysis of the magellan (magn) complementation group, that loss of function of the Drosophila polyubiquitin Ubi-p63E results specifically in meiotic arrest sterility in males. Ubi-p63E contributes predominantly to maintaining the free ubiquitin pool in testes. The function of Ubi-p63E is required cell-autonomously for proper meiotic chromatin condensation, cell cycle progression and spermatid differentiation. magn mutant germ cells develop normally to the spermatocyte stage but arrest at the G2/M transition of meiosis I, with lack of protein expression of the key meiotic cell cycle regulators Boule and Cyclin B. Loss of Ubi-p63E function did not strongly affect the spermatocyte transcription program regulated by the testis TBP-associated factor (tTAF) or meiosis arrest complex (tMAC) genes. Knocking down proteasome function specifically in spermatocytes caused a different meiotic arrest phenotype, suggesting that the magn phenotype might not result from general defects in protein degradation. Our results suggest a conserved role of polyubiquitin genes in male meiosis and a potential mechanism leading to meiosis I maturation arrest.

Indexed as

AnimalsBlotting, WesternCell CycleCell DifferentiationChromosome MappingCloning, MolecularDNA PrimersDrosophilaGerm CellsIn Situ HybridizationMaleMeiosisMicroarray AnalysisMicroscopy, FluorescencePolyubiquitinReverse Transcriptase Polymerase Chain ReactionDNA PrimersPolyubiquitinDrosophilaMeiosisSpermatocyteSpermatogenesisUbiquitin

Identifiers

PMID23884444
PMCPMC3742140
OpenAlexW2006307886

What OpenQuestion holds

Textmetadata
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.