ArticleMolecular genetics and genomics : MGG2011
DNA repair defects sensitize cells to anticodon nuclease yeast killer toxins.
Article in Molecular genetics and genomics : MGG, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- tRNA binding to Kti12 is crucial for wobble uridine modification by Elongator.Nucleic acids research · 2025Article
- Yeast geneMicrobial cell (Graz, Austria) · 2023Article
- Article
- Fungal Kti12 proteins display unusual linker regions and unique ATPase p-loops.Current genetics · 2020Article
- Kti12, a PSTK-like tRNA dependent ATPase essential for tRNA modification by Elongator.Nucleic acids research · 2019Article
- Protein Phosphatase Sit4 Affects Lipid Droplet Synthesis and Soraphen A Resistance Independent of Its Role in Regulating Elongator Dependent tRNA Modification.Biomolecules · 2018Article
- Article
- Codon-biased translation can be regulated by wobble-base tRNA modification systems during cellular stress responses.RNA biology · 2015Review
- Site-directed mutagenesis of the heterotrimeric killer toxin zymocin identifies residues required for early steps in toxin action.Applied and environmental microbiology · 2014Article
- Type I restriction enzymes and their relatives.Nucleic acids research · 2014Review
- The changing scene of amyotrophic lateral sclerosis.Nature reviews. Neuroscience · 2013Review
- Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Killer toxins from Kluyveromyces lactis (zymocin) and Pichia acaciae (PaT) were found to disable translation in target cells by virtue of anticodon nuclease (ACNase) activities on tRNA(Glu) and tRNA(Gln), respectively. Surprisingly, however, ACNase exposure does not only impair translation, but also affects genome integrity and concomitantly DNA damage occurs. Previously, it was shown that homologous recombination protects cells from ACNase toxicity. Here, we have analyzed whether other DNA repair pathways are functional in conferring ACNase resistance as well. In addition to HR, base excision repair (BER) and postreplication repair (PRR) promote clear resistance to either, PaT and zymocin. Comparative toxin sensitivity analysis of BER mutants revealed that its ACNase protective function is due to the endonucleases acting on apurinic (AP) sites, whereas none of the known DNA glycosylases is involved. Because PaT and zymocin require the presence of the ELP3/TRM9-dependent wobble uridine modification 5-methoxy-carbonyl-methyl (mcm(5)) for tRNA cleavage, we analyzed toxin response in DNA repair mutants additionally lacking such tRNA modifications. ACNase resistance caused by elp3 or trm9 mutations was found to rescue hypersensitivity of DNA repair defects, consistent with DNA damage to occur as a consequence of tRNA cleavage. The obtained genetic evidence promises to reveal new aspects into the mechanism linking translational fidelity and genome surveillance.
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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.