Evidence map›Paper›PMID 41326346›Full record

ArticleNature communications2025

Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.

Amador Romero-Franco, Cintia Checa-Rodríguez, Sonia Jimeno, Maikel Castellano-Pozo, Paula Aguilera, Hector Miras, Amadeo Wals, Silvia Jimeno-González, Andres Joaquin Lopez-Contreras, Pablo Huertas

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

10 authors.

Amador Romero-FrancoFacultad de Biología, Universidad de Sevilla, Sevilla, Spain.
Cintia Checa-Rodríguez *Facultad de Biología, Universidad de Sevilla, Sevilla, Spain.ORCID http://orcid.org/0000-0003-4838-7323
Sonia Jimeno *Facultad de Biología, Universidad de Sevilla, Sevilla, Spain.
Maikel Castellano-Pozo *Facultad de Biología, Universidad de Sevilla, Sevilla, Spain.ORCID http://orcid.org/0000-0003-4134-9025
Paula AguileraCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Sevilla, Spain.ORCID http://orcid.org/0000-0002-6937-8517
Hector MirasServicios de Oncología Radioterápica y de Radiofísica, Hospital Universitario Virgen Macarena, Sevilla, Spain.ORCID http://orcid.org/0000-0002-0534-3657
Amadeo WalsServicios de Oncología Radioterápica y de Radiofísica, Hospital Universitario Virgen Macarena, Sevilla, Spain.ORCID http://orcid.org/0000-0002-8869-1015
Silvia Jimeno-GonzálezFacultad de Biología, Universidad de Sevilla, Sevilla, Spain.ORCID http://orcid.org/0000-0002-6223-9573
Andres Joaquin Lopez-ContrerasCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Sevilla, Spain.ORCID http://orcid.org/0000-0002-5517-7327
Pablo HuertasFacultad de Biología, Universidad de Sevilla, Sevilla, Spain. phuertas@us.es.ORCID http://orcid.org/0000-0002-1756-4449

Funding

Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía (Ministry of Economy, Innovation, Science and Employment, Government of Andalucia) P18-RT-1204Fundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer) PRYGN246626HUERMinistry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2022-136791NB-I00
6 · The paper itself

Abstract

Genomic stability maintenance requires the repair of DNA breaks in the most accurate fashion. So, an exquisite regulatory network controls the choice between different repair mechanisms to maximize genome integrity. This relies mostly at the level of DNA end resection, the initial steps of the homologous recombination. On the other hand, numerous cellular activities follow a 24 h oscillation known as the circadian cycle. Thus, we explored the regulation of the choice between different DNA break repair pathways along the circadian cycle. Here we show that in human cells DNA resection shows a circadian oscillation, with a peak at early morning followed by a partial and progressive reduction until late afternoon. Such regulation depends on the circadian clock core component CRY1, which modulates the anti-resection activity of CCAR2 to limit CtIP at nightfall. Additionally, such regulation requires DNA-PK-mediated phosphorylation of CRY1. Finally, this circadian regulation impacts cancer progression and response to radiation therapy of specific tumours.

Indexed as

Circadian RhythmCryptochromesHomologous RecombinationCell Line, TumorCircadian ClocksDNADNA-Activated Protein KinaseDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairEndodeoxyribonucleasesHumansPhosphorylationCRY1 protein, humanCryptochromesDNADNA-Activated Protein KinaseDNA-Binding ProteinsEndodeoxyribonucleasesRBBP8 protein, human

Identifiers

PMID41326346
PMCPMC12669580

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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.