Evidence map›Paper›PMID 23258628›Full record

ArticleAndrology2013

Germ cell-specific disruption of the Meig1 gene causes impaired spermiogenesis in mice.

M E Teves, K N Jha, J Song, D R Nagarkatti-Gude, J C Herr, J A Foster, J F Strauss, Z Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Andrology, 2013. 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
1.4field-weighted citation impact, top 17% 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, 12 citations in OpenAlex.

  1. Article
  2. Identification and functional analysis ofFrontiers in physiology · 2022
    Article
  3. Article
  4. Sperm dysfunction and ciliopathy.Reproductive medicine and biology · 2016
    Review
  5. Article
  6. Article
  7. 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

8 authors at 3 institutions in 1 country.

M E TevesDepartment of Obstetrics & Gynecology, Virginia Commonwealth University, Richmond, VA 23298, USA.
K N Jha
J Song
D R Nagarkatti-Gude
J C Herr
J A Foster
J F Strauss
Z Zhang
Virginia Commonwealth University · USUniversity of Virginia · USRandolph–Macon College · US

Funding

VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
MOLECULAR BASIS OF MAMMALIAN SPERM MOTILITYR01HD037416 · NICHD · VIRGINIA COMMONWEALTH UNIVERSITY · PI STRAUSS, JEROME F · 2000 to 2010
$2.4M
Antimicrobial Proteins Secreted by the EpididymisR01HD045783 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI HERR, JOHN C · 2004 to 2008
$1.3M
Elucidating the role of Spag16, a bifunctional gene, in control of male fertilityF31HD062314 · NICHD · VIRGINIA COMMONWEALTH UNIVERSITY · PI NAGARKATTI-GUDE, DAVID ROBERT DE VELA · 2009 to 2011
$98k
NICHD NIH HHS 5F31HD062314NICHD NIH HHS F31 HD062314NICHD NIH HHS HD 045783NICHD NIH HHS HD37416NICHD NIH HHS R01 HD037416NICHD NIH HHS R01 HD045783NINDS NIH HHS 5P30NS047463NINDS NIH HHS P30 NS047463
6 · The paper itself

Abstract

Meiosis expressed gene 1 (Meig1) was originally identified in a search for mammalian genes potentially involved in meiosis. Seven mouse Meig1 transcripts with the same coding region, but different 5'-UTRs, have been identified. These transcripts have different tissue distributions, two are only present in the testis. In the testis, Meig1 is present in germ cells and Sertoli cells. A Meig1 conditional knockout model has been generated. When Meig1 was inactivated globally by crossing with Cmv-Cre transgenic mice, the Meig1-deficient males were sterile due to severe spermiogenic defects, and had no obvious defects in meiosis. To further study its role in individual cell types in the testis, the Meig1(flox) mice were crossed with Hsp2a-Cre, Prm-Cre, and Amh-Cre mice, in which the Cre recombinase is driven by the heat shock protein 2 (Hsp2a) gene promoter (expressed in spermatocytes), the protamine 1 gene promoter (expressed in post-meiotic spermatids) and the anti-Mullerian hormone (Amh) gene promoter (expressed in Sertoli cells) respectively. Both Meig1 mRNA and protein were undetectable in testis of the Hsp2a-Cre; Meig1(flox/flox) mice and all the mutant adult males tested were sterile. This phenotype mirrors that of the Cmv-Cre; Meig1(flox/flox) mice. Even though the total testicular Meig1 mRNA and protein expression levels were dramatically reduced in testis of the Prm-Cre; Meig1(flox/flox) males, all the mice tested were fertile, and there was no significant difference in sperm count and sperm motility compared with age-matched Meig1(flox/flox) male mice. Disruption of Meig1 in the Sertoli cells did not affect the MEIG1 protein expression. Amh-Cre; Meig1(flox/flox) males were fertile, and produced the same amount of spermatozoa as age-matched Meig1(flox/flox) mice. The testicular histology was also normal. Our results indicate that MEIG1 regulates spermiogenesis through effects in germ cells alone, and that the Meig1 gene must be active during a discrete period in spermatogenesis after which it is dispensable.

Indexed as

SpermatogenesisAnimalsAnti-Mullerian HormoneCell Cycle ProteinsFemaleFertilityGenotypeHeat-Shock ProteinsInfertility, MaleLitter SizeMaleMeiosisMiceMice, KnockoutMice, TransgenicNuclear ProteinsAnti-Mullerian HormoneCell Cycle ProteinsHeat-Shock ProteinsHsf2 protein, mouseMeig1 protein, mouseNuclear ProteinsPhosphoproteinsRNA, MessengerTranscription Factors

Identifiers

PMID23258628
PMCPMC4120260
OpenAlexW1981128560

What OpenQuestion holds

Textmetadata
LicenceTDM
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.