Evidence map›Paper›PMID 25979708›Full record

ArticleBiology open2015

BAZ1B is dispensable for H2AX phosphorylation on Tyrosine 142 during spermatogenesis.

Tyler J Broering, Yuan-Liang Wang, Ram Naresh Pandey, Rashmi S Hegde, Shao-Chun Wang, Satoshi H Namekawa

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. SMARCA5 restricts chromatin accessibility to promote male meiosis and fertility in mammals.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The multi-functional eyes absent proteins.Critical reviews in biochemistry and molecular biology · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Chromosome Spread Analyses of Meiotic Sex Chromosome Inactivation.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  12. 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

6 authors at 2 institutions in 2 countries.

Tyler J BroeringDivision of Reproductive Sciences, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Division of Developmental Biology, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Yuan-Liang WangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Ram Naresh PandeyDivision of Developmental Biology, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Rashmi S HegdeDivision of Developmental Biology, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Shao-Chun WangDepartment of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
Satoshi H NamekawaDivision of Reproductive Sciences, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Division of Developmental Biology, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA satoshi.namekawa@cchmc.org.
Perinatal Institute · GBUniversity of Cincinnati Medical Center · US

Funding

Molecular Mechanisms of Retinal Determination ProteinsR01EY014648 · NEI · CINCINNATI CHILDRENS HOSP MED CTR · PI HEGDE, RASHMI S. · 2004 to 2017
$4.1M
DNA Damage Response Pathways in Meiotic Sex Chromosome InactivationR01GM098605 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI NAMEKAWA, SATOSHI · 2011 to 2020
$3.3M
EYA in Retinal AngiogenesisR01EY022917 · NEI · CINCINNATI CHILDRENS HOSP MED CTR · PI HEGDE, RASHMI S. · 2013 to 2016
$1.5M
Early exposure to phthalate & obesity: the role of PCNA tyrosine phosphorylationR21ES023942 · NIEHS · UNIVERSITY OF CINCINNATI · PI WALTZ, SUSAN E · 2015 to 2016
$435k
NEI NIH HHS R01 EY014648NEI NIH HHS R01 EY022917NIEHS NIH HHS R21 ES023942NIGMS NIH HHS R01 GM098605
6 · The paper itself

Abstract

Meiosis is precisely regulated by the factors involved in DNA damage response in somatic cells. Among them, phosphorylation of H2AX on Serine 139 (γH2AX) is an essential signal for the silencing of unsynapsed sex chromosomes during male meiosis. However, it remains unknown how adjacent H2AX phosphorylation on Tyrosine 142 (pTyr142) is regulated in meiosis. Here we investigate the meiotic functions of BAZ1B (WSTF), the only known Tyr142 kinase in somatic cells, using mice possessing a conditional deletion of BAZ1B. Although BAZ1B deletion causes ectopic γH2AX signals on synapsed autosomes during the early pachytene stage, BAZ1B is dispensable for fertility and critical events during spermatogenesis. BAZ1B deletion does not alter events on unsynapsed axes and pericentric heterochromatin formation. Furthermore, BAZ1B is dispensable for localization of the ATP-dependent chromatin remodeling protein SMARCA5 (SNF2h) during spermatogenesis despite the complex formation between BAZ1B and SMARCA5, known as the WICH complex, in somatic cells. Notably, pTyr142 is regulated independently of BAZ1B and is dephosphorylated on the sex chromosomes during meiosis in contrast with the presence of adjacent γH2AX. Dephosphorylation of pTyr142 is regulated by MDC1, a binding partner of γH2AX. These results reveal the distinct regulation of two adjacent phosphorylation sites of H2AX during meiosis, and suggest that another kinase mediates Tyr142 phosphorylation.

Indexed as

MeiosisSex chromosomesSpermatogenesis

Identifiers

PMID25979708
PMCPMC4571090
OpenAlexW2158362186

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.