ArticleMolecular and cellular biology2009
TOR complex 2 controls gene silencing, telomere length maintenance, and survival under DNA-damaging conditions.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- TORC2 coordinates MBF-dependent transcription and restrains oxidative stress responses during DNA replication stress in fission yeast.The Journal of biological chemistry · 2026Article
- A time-resolved high-throughput screening of fission yeast deletion mutants for oxidative stress resistance.Microbial cell (Graz, Austria) · 2026Article
- TORC2 inactivation promotes heterochromatin formation in rDNA and prolongs viability of quiescent fission yeast cells.Communications biology · 2025Article
- Acrylamide-mediated errors in the cell cycle regulation are associated with altered TORC2 signaling in Schizosaccharomyces pombe.Scientific reports · 2025Article
- Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast.Microbial cell (Graz, Austria) · 2025Article
- TOR complex 2 contributes to regulation of gene expression via inhibiting Gcn5 recruitment to subtelomeric and DNA replication stress genes.PLoS genetics · 2022Article
- A comparative analysis of telomere length maintenance circuits in fission and budding yeast.Frontiers in genetics · 2022Article
- Genes affecting the extension of chronological lifespan in Schizosaccharomyces pombe (fission yeast).Molecular microbiology · 2021Review
- Review
- Nuclear F-actin counteracts nuclear deformation and promotes fork repair during replication stress.Nature cell biology · 2020Article
- TOR Complex 2- independent mutations in the regulatory PIF pocket of Gad8AKT1/SGK1 define separate branches of the stress response mechanisms in fission yeast.PLoS genetics · 2020Article
- Review
- Review
- The TOR pathway modulates cytoophidium formation inThe Journal of biological chemistry · 2019Article
- Mck1 defines a key S-phase checkpoint effector in response to various degrees of replication threats.PLoS genetics · 2019Article
- Transposable element insertions in fission yeast drive adaptation to environmental stress.Genome research · 2019Article
- TOR complex 2 in fission yeast is required for chromatin-mediated gene silencing and assembly of heterochromatic domains at subtelomeres.The Journal of biological chemistry · 2018Article
- Express yourself: how PP2A-B55Current genetics · 2018Review
- Review
- mTORC1 and -2 Coordinate Transcriptional and Translational Reprogramming in Resistance to DNA Damage and Replicative Stress in Breast Cancer Cells.Molecular and cellular biology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The Target Of Rapamycin (TOR) kinase belongs to the highly conserved eukaryotic family of phosphatidylinositol-3-kinase-related kinases (PIKKs). TOR proteins are found at the core of two distinct evolutionarily conserved complexes, TORC1 and TORC2. Disruption of TORC1 or TORC2 results in characteristically dissimilar phenotypes. TORC1 is a major cell growth regulator, while the cellular roles of TORC2 are not well understood. In the fission yeast Schizosaccharomyces pombe, Tor1 is a component of the TORC2 complex, which is particularly required during starvation and various stress conditions. Our genome-wide gene expression analysis of Deltator1 mutants indicates an extensive similarity with chromatin structure mutants. Consistently, TORC2 regulates several chromatin-mediated functions, including gene silencing, telomere length maintenance, and tolerance to DNA damage. These novel cellular roles of TORC2 are rapamycin insensitive. Cells lacking Tor1 are highly sensitive to the DNA-damaging drugs hydroxyurea (HU) and methyl methanesulfonate, similar to mutants of the checkpoint kinase Rad3 (ATR). Unlike Rad3, Tor1 is not required for the cell cycle arrest in the presence of damaged DNA. Instead, Tor1 becomes essential for dephosphorylation and reactivation of the cyclin-dependent kinase Cdc2, thus allowing reentry into mitosis following recovery from DNA replication arrest. Taken together, our data highlight critical roles for TORC2 in chromatin metabolism and in promoting mitotic entry, most notably after recovery from DNA-damaging conditions. These data place TOR proteins in line with other PIKK members, such as ATM and ATR, as guardians of genome stability.
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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.