ArticleNucleic acids research2015
Fungal Ku prevents permanent cell cycle arrest by suppressing DNA damage signaling at telomeres.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Systematic evaluation of the DNA repair machinery facilitated the development of efficient genome editing tools for the red yeastSynthetic and systems biotechnology · 2027Article
- Fungal DNA damage repair: from model to driver of virulence and AMR.Bioscience reports · 2026Review
- Exploring the intersection between necromass reutilization and genome protection reveals novel proteins that contribute to both processes in Ustilago maydis.Biology direct · 2026Article
- The yeast CST and Polα/primase complexes act in concert to ensure proper telomere maintenance and protection.Nucleic acids research · 2025Article
- Considerations for Domestication of Novel Strains of Filamentous Fungi.ACS synthetic biology · 2025Review
- Ustilago maydis Trf2 ensures genome stability by antagonizing Blm-mediated telomere recombination: Fine-tuning DNA repair factor activity at telomeres through opposing regulations.PLoS genetics · 2024Article
- Analysis of the indispensable RAD51 cofactor BRCA2 inLife science alliance · 2024Article
- Noncanonical functions of Ku may underlie essentiality in human cells.Scientific reports · 2023Article
- The contribution of DNA repair pathways to genome editing and evolution in filamentous pathogens.FEMS microbiology reviews · 2022Review
- Ustilago maydis telomere protein Pot1 harbors an extra N-terminal OB fold and regulates homology-directed DNA repair factors in a dichotomous and context-dependent manner.PLoS genetics · 2022Article
- Homology length dictates the requirement for Rad51 and Rad52 in gene targeting in the Basidiomycota yeast Naganishia liquefaciens.Current genetics · 2021Article
- The Ku complex: recent advances and emerging roles outside of non-homologous end-joining.Cellular and molecular life sciences : CMLS · 2021Review
- Structurally distinct telomere-binding proteins in Ustilago maydis execute non-overlapping functions in telomere replication, recombination, and protection.Communications biology · 2020Article
- Bioavailability of Nutritional Resources From Cells Killed by Oxidation Supports Expansion of Survivors inFrontiers in microbiology · 2018Article
- Protection of Arabidopsis Blunt-Ended Telomeres Is Mediated by a Physical Association with the Ku Heterodimer.The Plant cell · 2017Article
- Telomere recombination pathways: tales of several unhappy marriages.Current genetics · 2017Review
- Mre11 and Blm-Dependent Formation of ALT-Like Telomeres in Ku-Deficient Ustilago maydis.PLoS genetics · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The Ku heterodimer serves in the initial step in repairing DNA double-strand breaks by the non-homologous end-joining pathway. Besides this key function, Ku also plays a role in other cellular processes including telomere maintenance. Inactivation of Ku can lead to DNA repair defects and telomere aberrations. In model organisms where Ku has been studied, inactivation can lead to DNA repair defects and telomere aberrations. In general Ku deficient mutants are viable, but a notable exception to this is human where Ku has been found to be essential. Here we report that similar to the situation in human Ku is required for cell proliferation in the fungus Ustilago maydis. Using conditional strains for Ku expression, we found that cells arrest permanently in G2 phase when Ku expression is turned off. Arrest results from cell cycle checkpoint activation due to persistent signaling via the DNA damage response (DDR). Our results point to the telomeres as the most likely source of the DNA damage signal. Inactivation of the DDR makes the Ku complex dispensable for proliferation in this organism. Our findings suggest that in U. maydis, unprotected telomeres arising from Ku depletion are the source of the signal that activates the DDR leading to cell cycle arrest.
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Registered trials
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.