ArticleNucleic acids research2017
The RNA binding protein Npl3 promotes resection of DNA double-strand breaks by regulating the levels of Exo1.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The multiple layers of RNA response in double-strand break repair.Experimental & molecular medicine · 2025Review
- Proteasome-mediated degradation of long-range nucleases negatively regulates resection of DNA double-strand breaks.iScience · 2024Article
- RNA recognition by Npl3p reveals U2 snRNA-binding compatible with a chaperone role during splicing.Nature communications · 2023Article
- The mRNA export adaptor Yra1 contributes to DNA double-strand break repair through its C-box domain.PloS one · 2019Article
- Local unwinding of double-strand DNA ends by the MRX complex promotes Exo1 processing activity.Molecular & cellular oncology · 2018Article
- EXO1 overexpression is associated with poor prognosis of hepatocellular carcinoma patients.Cell cycle (Georgetown, Tex.) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells preserve genome integrity upon DNA damage by activating a signaling network that promotes DNA repair and controls cell cycle progression. One of the most severe DNA damage is the DNA double-strand break (DSB), whose 5΄ ends can be nucleolitically resected by multiple nucleases to create 3΄-ended single-stranded DNA tails that trigger DSB repair by homologous recombination. Here, we identify the Saccharomyces cerevisiae RNA binding protein Npl3 as a new player in DSB resection. Npl3 is related to both the metazoan serine-arginine-rich and the heterogeneous nuclear ribonucleo-proteins. NPL3 deletion impairs the generation of long ssDNA tails at the DSB ends, whereas it does not exacerbate the resection defect of exo1Δ cells. Furthermore, either the lack of Npl3 or the inactivation of its RNA-binding domains causes decrease of the exonuclease Exo1 protein levels as well as generation of unusual and extended EXO1 RNA species. These findings, together with the observation that EXO1 overexpression partially suppresses the resection defect of npl3Δ cells, indicate that Npl3 participates in DSB resection by promoting the proper biogenesis of EXO1 mRNA.
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