Lovastatin Triggers an Apoptosis-like Cell Death Process in the FungusMucor racemosus
Abstract
The filamentous dimorphic fungus Mucor racemosus possesses three ras genes, Mras1, 2, and 3, whose expression is correlated to morphogenesis of the fungus. Lovastatin, an indirect inhibitor of protein prenylation, altered the processing of MRas1 protein, blocked the accumulation of MRas3 protein, and caused the MRas1/p20 protein complex to disappear in M. racemosus. Concurrently it arrested sporangiospore germination, decreased growth rate, caused a loss of cell viability accompanied by cell shrinkage, increased cell density and cytoplasm condensation, and triggered DNA fragmentation, resulting in nucleosomes and nucleosome multimers. The specific morphological and biochemical events seen in Mucor cell death, particularly DNA fragmentation, resemble the best known characteristics of classical apoptosis in mammalian cells and prompted us to classify lovastatin-induced cell death as an apoptosis-like process. Lovastatin did not cause cell death in a leucine auxotroph of Mucor grown in YNB minimal medium, conditions which support only spherical growth during spore germination. Exogenous dibutyryl-cAMP initiated morphogenesis from hyphal (polar) growth to yeast-like (spherical) growth during spore germination and strongly prevented cell death which resulted from lovastatin treatment. Wortmannin added together with dibutyryl-cAMP showed a synergistic effect in the prevention of fungal cell death. These data suggest that the regulation of lovastatin-induced cell death in Mucor requires a signal transduction pathway(s) involving cAMP whose function is specific to a particular developmental stage.
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Lovastatin induces cell death resembling apoptosis in Mucor racemosus.
“Additionally, Roze et al. [119] found that lovastatin induces cell death resembling apoptosis in Mucor racemosus.”
From Statins as Antifungal Agents: A Review on Drug Repurposing and Nanotechnology-Driven Delivery Strategies (2025) · cites this paper as [119]
Lovastatin triggers DNA fragmentation in Mucor racemosus, resulting in the formation of nucleosomes and multimers.
“It also triggers DNA fragmentation, resulting in the formation of nucleosomes and multimers.”
From Statins as Antifungal Agents: A Review on Drug Repurposing and Nanotechnology-Driven Delivery Strategies (2025) · cites this paper as [119]
Lovastatin halts sporangiospore germination, reduces cell growth, and causes loss of viability in Mucor racemosus.
“Lovastatin halts sporangiospore germination, reduces cell growth, and causes loss of viability characterized by cell shrinkage, increased density, and cytoplasmic condensation.”
From Statins as Antifungal Agents: A Review on Drug Repurposing and Nanotechnology-Driven Delivery Strategies (2025) · cites this paper as [119]
LOV does not cause apoptotic cell death in yeasts compared to filamentous fungi.
“LOV does not cause apoptotic cell death in yeasts compared to filamentous fungi [24,31] .”
From Statins as antifungal agents (2011) · cites this paper as [31]
Statins induce apoptosis-like cell death in filamentous fungi.
“Beyond to the harmful effects on membrane fluidity and the synthesis of important isoprenoids for cell signaling and vital processes (such as cell proliferation and differentiation), and protein prenylation [16] , statins induce apoptosis-like cell death in filamentous fungi [15,30,31] .”
From Statins as antifungal agents (2011) · cites this paper as [31]
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- Authors
- Roze, L. V., & Linz, J. E.
- Affiliations
- Michigan State University (US)
- ORCID
- Venue
- Fungal Genetics and Biology
- Publisher
- Elsevier BV
- Published
- 1998-11
- Volume
- 25
- Issue
- 2
- Pages
- 119-133
- ISSN
- 1087-1845 (ISSN-L)
- OpenAlex
- W2010482423
- Cited by
- 96
- References
- 0
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 3 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 8 · 2014: 7 · 2013: 1 · 2012: 1
- FWCI
- 1.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Fungal Genetics and Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01gm041216-04)
- National Institute of General Medical Sciences (SROI GM 41216)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Keywords
- lovastatin, Mucor racemosus, apoptosis-like cell death, ras gene, protein prenylation, DNA fragmentation, sporangiospore germination, fungal morphogenesis, cAMP signaling, wortmannin, dibutyryl cyclic AMP, signal transduction, dimorphic fungi
- MeSH terms
- Wortmannin, Androstadienes, Antifungal Agents, Bucladesine, Genes, Fungal, Kinetics, Lovastatin, Mucor, Genes, ras, Sphingosine, Cell Death, Apoptosis, DNA Fragmentation
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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