The TOR Pathway Plays Pleiotropic Roles in Growth and Stress Responses of the Fungal Pathogen Cryptococcus neoformans
Open accessAbstract
The target of rapamycin (TOR) pathway is an evolutionarily conserved signal transduction system that governs a plethora of eukaryotic biological processes, but its role in Cryptococcus neoformans remains elusive. In this study, we investigated the TOR pathway by functionally characterizing two Tor-like kinases, Tor1 and Tlk1, in C. neoformans. We successfully deleted TLK1, but not TOR1. TLK1 deletion did not result in any evident in vitro phenotypes, suggesting that Tlk1 is dispensable for the growth of C. neoformans. We demonstrated that Tor1, but not Tlk1, is essential and the target of rapamycin by constructing and analyzing conditionally regulated strains and sporulation analysis of heterozygous mutants in the diploid strain background. To further analyze the Tor1 function, we constructed constitutive TOR1 overexpression strains. Tor1 negatively regulated thermotolerance and the DNA damage response, which are two important virulence factors of C. neoformans. TOR1 overexpression reduced Mpk1 phosphorylation, which is required for cell wall integrity and thermoresistance, and Rad53 phosphorylation, which governs the DNA damage response pathway. Tor1 is localized to the cytoplasm, but enriched in the vacuole membrane. Phosphoproteomics and transcriptomics revealed that Tor1 regulates a variety of biological processes, including metabolic processes, cytoskeleton organization, ribosome biogenesis, and stress response. TOR inhibition by rapamycin caused actin depolarization in a Tor1-dependent manner. Finally, screening rapamycin-sensitive and -resistant kinase and transcription factor mutants revealed that the TOR pathway may crosstalk with a number of stress signaling pathways. In conclusion, our study demonstrates that a single Tor1 kinase plays pleiotropic roles in C. neoformans.
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Evidence exists for divergence in regulation of TOR signalling in C. neoformans and other fungi.
“However, evidence exists for divergence in regulation of TOR signalling in C. neoformans and other fungi85, which would have important implications for the development of a broad-spectrum antifungal therapeutic.”
From Treatment strategies for cryptococcal infection: challenges, advances and future outlook (2021) · cites this paper as [85]
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Self-citation
- Authors
- So, Y.-S., Lee, D.-G., Idnurm, A., Ianiri, G., & Bahn, Y.-S.
- Affiliations
- Yonsei University (KR)
- The University of Melbourne (AU)
- Duke Medical Center (US)
- Corresponding author
- Bahn, Yong-Sun
- Venue
- Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-06-07
- Volume
- 212
- Issue
- 4
- Pages
- 1241-1258
- ISSN
- 0016-6731 (ISSN-L)
- 1943-2631
- PMC
- PMC6707454
- OpenAlex
- W2948105229
- Cited by
- 36
- References
- 54
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 7 · 2023: 3 · 2022: 5 · 2021: 7 · 2020: 3
- FWCI
- 2.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Genetics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi del Molise (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R21AI094364)
- Topics
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- TOR signaling, Cryptococcus neoformans, heat tolerance, DNA damage response, Rad53 phosphorylation, cell wall integrity, virulence factors, rapamycin sensitivity
- MeSH terms
- Thermotolerance, Mechanistic Target of Rapamycin Complex 1, Cryptococcus neoformans, Cytoskeleton, Fungal Proteins, Ribosomes, Spores, Fungal, Signal Transduction, Genetic Pleiotropy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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