Evidence map›Paper›PMID 23788429›Full record

ArticleJournal of cell science2013

The DNA damage checkpoint protein RAD9A is essential for male meiosis in the mouse.

Ana Vasileva, Kevin M Hopkins, Xiangyuan Wang, Melissa M Weisbach, Richard A Friedman, Debra J Wolgemuth, Howard B Lieberman

Abstract read
In one paragraph

Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Parasitic castration by a viral protein tyrosine phosphatase targeting the host cell cycle checkpoint protein Rad9A.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Transcriptional profiles analysis of effects ofFrontiers in cellular and infection microbiology · 2024
    Article
  6. Double strand DNA breaks in sperm: the bad guy in the crowd.Journal of assisted reproduction and genetics · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The meiotic checkpoint network: step-by-step through meiotic prophase.Cold Spring Harbor perspectives in biology · 2014
    Review
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

7 authors at 1 institution in 1 country.

Ana VasilevaCenter for Radiological Research, College of Physicians and Surgeons, Columbia University Medical Center, New York, NY 10032, USA.
Kevin M Hopkins
Xiangyuan Wang
Melissa M Weisbach
Richard A Friedman
Debra J Wolgemuth
Howard B Lieberman
Columbia University Irving Medical Center · US

Funding

Mechanisms of Radioresistance and Cell Cycle ProgressionR01CA130536 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2007 to 2016
$3.5M
The MRAD9 Radioresistance GeneR01GM079107 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEBERMAN, HOWARD B. · 2006 to 2013
$2.6M
NCI NIH HHS R01 CA130536NCI NIH HHS R01CA130536NIGMS NIH HHS R01 GM079107NIGMS NIH HHS R01GM079107
6 · The paper itself

Abstract

In mitotic cells, RAD9A functions in repairing DNA double-strand breaks (DSBs) by homologous recombination and facilitates the process by cell cycle checkpoint control in response to DNA damage. DSBs occur naturally in the germline during meiosis but whether RAD9A participates in repairing such breaks is not known. In this study, we determined that RAD9A is indeed expressed in the male germ line with a peak of expression in late pachytene and diplotene stages, and the protein was found associated with the XY body. As complete loss of RAD9A is embryonic lethal, we constructed and characterized a mouse strain with Stra8-Cre driven germ cell-specific ablation of Rad9a beginning in undifferentiated spermatogonia in order to assess its role in spermatogenesis. Adult mutant male mice were infertile or sub-fertile due to massive loss of spermatogenic cells. The onset of this loss occurs during meiotic prophase, and there was an increase in the numbers of apoptotic spermatocytes as determined by TUNEL. Spermatocytes lacking RAD9A usually arrested in meiotic prophase, specifically in pachytene. The incidence of unrepaired DNA breaks increased, as detected by accumulation of γH2AX and DMC1 foci on the axes of autosomal chromosomes in pachytene spermatocytes. The DNA topoisomerase IIβ-binding protein 1 (TOPBP1) was still localized to the sex body, albeit with lower intensity, suggesting that RAD9A may be dispensable for sex body formation. We therefore show for the first time that RAD9A is essential for male fertility and for repair of DNA DSBs during meiotic prophase I.

Indexed as

DNA Breaks, Double-StrandedAdaptor Proteins, Signal TransducingAnimalsApoptosisCarrier ProteinsCell Cycle CheckpointsCell Cycle ProteinsFertilityHistonesMaleMeiotic Prophase IMiceMice, TransgenicNuclear ProteinsPhosphate-Binding ProteinsRecombinational DNA RepairAdaptor Proteins, Signal TransducingCarrier ProteinsCell Cycle ProteinsDmc1 protein, mousegamma-H2AX protein, mouseHistonesNuclear ProteinsPhosphate-Binding Proteinsrad9 proteinStra8 protein, mouseTopbp1 protein, mouseDouble-strand breaksMeiosisRAD9ASpermatogenesis

Identifiers

PMID23788429
PMCPMC3757332
OpenAlexW2077086709

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.