Multifactorial Role of Mitochondria in Echinocandin Tolerance Revealed by Transcriptome Analysis of Drug-Tolerant Cells
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Abstract
Echinocandin drugs are a first-line therapy to treat invasive candidiasis, which is a major source of morbidity and mortality worldwide. The opportunistic fungal pathogen Candida glabrata is a prominent bloodstream fungal pathogen, and it is notable for rapidly developing echinocandin-resistant strains associated with clinical failure.
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That same study also tested "mitochondrial inhibitors" that either have multiple cellular targets or have no targets at all in C. glabrata, producing data that did not match the mitochondria-deficient mutants.
“That same study also tested “mitochondrial inhibitors” that either have multiple cellular targets (sodium azide) or have no targets at all in C. glabrata (diphenyleneiodonium chloride, rotenone), producing data that did not match the mitochondria-deficient mutants.”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [47]
The Results section (page unavailable) confirms that the study tested rotenone, DPI, and sodium azide and found that inhibitor treatment and mitochondrial defects had different effects on caspofungin tolerance. But the Discussion identifies DPI as an inhibitor of NADH dehydrogenases and sodium azide as an inhibitor of complex IV; it does not support describing DPI as having no target or sodium azide as having multiple cellular targets in C. glabrata. It notes that C. glabrata lacks rotenone’s canonical complex I target, while suggesting rotenone may also act through other pathways. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThat conclusion is inconsistent with the genetic data reported there and here, showing that several mitochondria-deficient knockout mutants exhibited wild-type levels of viability after long exposure to high doses of echinocandins.
“That conclusion is inconsistent with the genetic data reported there (47) and here (Fig. S4), showing that several mitochondria-deficient knockout mutants (cox4∆, atp1∆, atp2∆, atp10∆, mrp20∆) exhibited wild-type levels of viability after long exposure to high doses of echinocandins.”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [47]
The Results section (page unavailable) reports 24-hour caspofungin survival assays involving cox4Δ, atp1Δ, atp2Δ, and atp10Δ. It describes these mutants as less tolerant at one or more concentrations, particularly below the MIC, but does not state that they had wild-type viability at high doses. The paper also does not report an mrp20Δ mutant; the citing sentence attributes data from the citing paper’s own Fig. S4 as well. (LLM, conf=0.84)
Experimental — accuracy not yet measuredA recent study concluded that mitochondrial dysfunction decreases tolerance to echinocandins in C. glabrata.
“A recent study concluded that mitochondrial dysfunction decreases tolerance to echinocandins in C. glabrata (47).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [47]
The Discussion (Fig. 8) says chronic mitochondrial dysfunction decreases echinocandin tolerance in C. glabrata. But the Discussion also distinguishes this from acute mitochondrial inhibition, which reduced echinocandin-mediated killing. The claim omits that important qualification. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe recent report did not make use of time-kill experiments and extensively utilized low-resolution dose-kill experiments.
“The recent report (47) did not make use of time-kill experiments and extensively utilized low-resolution dose-kill experiments, in which CFU are quantified at only one time point (24 h) after exposure to varying doses of echinocandins (23).”
From Echinocandin tolerance and persistence <i>in vitro</i> are regulated by calcineurin signaling in <i>Candida glabrata</i> (2026) · cites this paper as [47]
Caspofungin stress itself can induce reactive oxygen species (ROS) accumulation, which has been linked to decreased susceptibility and may act as a driver of lipid peroxidation.
“caspofungin stress itself can induce reactive oxygen species (ROS) accumulation [54], which has been linked to decreased susceptibility and may act as a driver of lipid peroxidation”
From Calcineurin‐Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in <i>Candida Glabrata</i> (2026) · cites this paper as [54]
A higher tolerance to ER stress has already been described for other petite C. glabrata isolates.
“A higher tolerance to ER stress has already been described for other petite C. glabrata isolates (6).”
From Overlooked <i>Candida glabrata</i> petites are echinocandin tolerant, induce host inflammatory responses, and display poor <i>in vivo</i> fitness (2023) · cites this paper as [6]
The Discussion (page unavailable) describes petite C. glabrata mutants lacking susceptibility to oxidative stress under hydrogen peroxide, not increased tolerance to endoplasmic reticulum (ER) stress. Searches for ER stress, endoplasmic reticulum stress, and tunicamycin found no passage in our copy addressing the claimed ER-stress tolerance. (LLM, conf=0.76)
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“A higher tolerance to ER stress has already been described for other petite C. glabrata isolates (6).”
BackgroundMethodInfluentialSelf-citationHistone Acetylation Regulator Gcn5 Mediates Drug Resistance and Virulence of Candida glabrata
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“The recent report (47) did not make use of time-kill experiments and extensively utilized low-resolution dose-kill experiments, in which CFU are quantified at only one time point (24 h) after exposure to varying doses of echinocandins (23).”
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Core histones govern echinocandin susceptibility in Candida glabrata
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Adaptively evolved chitin overproduction in Saccharomyces cerevisiae
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- Authors
- Garcia-Rubio, R., Jimenez-Ortigosa, C., DeGregorio, L., Quinteros, C., Shor, E., & Perlin, D. S.
- Affiliations
- Center for Discovery and Innovation, Hackensack Meridian Health, Nutley, New Jersey, USA
- Hackensack Meridian Health (US)
- Georgetown University (US)
- Corresponding author
- Shor, Erika
- Perlin, David S.
- Venue
- mBio
- Publisher
- American Society for Microbiology
- Published
- 2021-08-31
- Volume
- 12
- Issue
- 4
- Pages
- e0195921-e0195921
- ISSN
- 2150-7511 (ISSN-L)
- PMC
- PMC8406274
- OpenAlex
- W3189016689
- Cited by
- 29
- References
- 73
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 1
- FWCI
- 1.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- mBio (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- HHS | National Institutes of Health (5R01AI109025)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
- Keywords
- Candida glabrata, mitochondrial function, echinocandin resistance, invasive candidiasis, electron transport inhibition, gene expression signatures, antifungal resistance, fungemia
- MeSH terms
- Antifungal Agents, Microbial Sensitivity Tests, Mitochondria, Stress, Physiological, Gene Expression Profiling, Candida glabrata, Echinocandins
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