Evidence map›Paper›PMID 23857907›Full record

ArticleJournal of cell science2013

Ku70 and non-homologous end joining protect testicular cells from DNA damage.

Emad A Ahmed, Agnel Sfeir, Hiroyuki Takai, Harry Scherthan

Open access · bronzeAbstract 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
1.0field-weighted citation impact, top 24% 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, 50 citations in OpenAlex.

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  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

4 authors at 3 institutions in 2 countries.

Emad A AhmedInstitut für Radiobiologie der Bundeswehr in Verbindung mit der Universität, Ulm, Neuherbergstrasse 1, D-80937 München, Germany.
Agnel Sfeir
Hiroyuki Takai
Harry Scherthan
Rockefeller University · USInstitut für Radiobiologie der BundeswehrMax Planck Institute for Molecular Genetics · DE

Funding

MECHANISMS OF TELOMERE INDUCED SENESCENCER01AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI Titia de Lange · 1999 to 2026
$11.9M
Molecular Cytology of Human Telomeres: Telomere proteinR37GM049046 · NIGMS · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 2005 to 2014
$5.0M
MOLECULAR CYTOLOGY OF HUMAN TELOMERES--TELOMERE PROTEINR01GM049046 · NIGMS · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 1993 to 2004
$1.8M
Mechanism of the telomeric proliferation limitR56AG016642 · NIA · ROCKEFELLER UNIVERSITY · PI DE LANGE, TITIA · 2019 to 2019
$598k
NIA NIH HHS AG016642NIA NIH HHS R01 AG016642NIA NIH HHS R56 AG016642NIGMS NIH HHS GM049046NIGMS NIH HHS R01 GM049046NIGMS NIH HHS R37 GM049046
6 · The paper itself

Abstract

Spermatogenesis is a complex process that generates haploid germ cells or spores and implements meiosis, a succession of two special cell divisions that are required for homologous chromosome segregation. During prophase to the first meiotic division, homologous recombination (HR) repairs Spo11-dependent DNA double-strand breaks (DSBs) in the presence of telomere movements to allow for chromosome pairing and segregation at the meiosis I division. In contrast to HR, non-homologous end joining (NHEJ), the major DSB repair mechanism during the G1 cell cycle phase, is downregulated during early meiotic prophase. At somatic mammalian telomeres, the NHEJ factor Ku70/80 inhibits HR, as does the Rap1 component of the shelterin complex. Here, we investigated the role of Ku70 and Rap1 in meiotic telomere redistribution and genome protection in spermatogenesis by studying single and double knockout mice. Ku70(-/-) mice display reduced testis size and compromised spermatogenesis, whereas meiotic telomere dynamics and chromosomal bouquet formation occurred normally in Ku70(-/-) and Ku70(-/-)Rap1(Δ/Δ) knockout spermatocytes. Elevated mid-preleptotene frequencies were associated with significantly increased DNA damage in Ku-deficient B spermatogonia, and in differentiated Sertoli cells. Significantly elevated levels of γH2AX foci in Ku70(-/-) diplotene spermatocytes suggest compromised progression of DNA repair at a subset of DSBs. This might explain the elevated meiotic metaphase apoptosis that is present in Ku70-deficient stage XII testis tubules, indicating spindle assembly checkpoint activation. In summary, our data indicate that Ku70 is important for repairing DSBs in somatic cells and in late spermatocytes of the testis, thereby assuring the fidelity of spermatogenesis.

Indexed as

DNA DamageSpermatogenesisAnimalsAntigens, NuclearApoptosisCell CycleCells, CulturedDNA-Binding ProteinsDNA, RecombinantDNA RepairKu AutoantigenMaleMeiosisMiceMice, Inbred C57BLMice, KnockoutAntigens, NuclearDNA-Binding ProteinsDNA, RecombinantKu Autoantigenrap1 GTP-Binding ProteinsXrcc6 protein, mouseBouquet formationDNA damageKu70MeiosisMid-preleptoteneNHEJRap1RecombinationSertoli cellShelterinSpermatogenesisTelomere attachment

Identifiers

PMID23857907
PMCPMC3711201
OpenAlexW2053264334

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.