ArticleFungal genetics and biology : FG & B2012
Arv1 lipid transporter function is conserved between pathogenic and nonpathogenic fungi.
Article in Fungal genetics and biology : FG & B, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Insights intomSphere · 2026Article
- An Erg11 lanosterol 14-α-demethylase-Arv1 complex is required for Candida albicans virulence.PloS one · 2020Article
- Candida albicans gains azole resistance by altering sphingolipid composition.Nature communications · 2018Article
- Mice lackingThe Journal of biological chemistry · 2018Article
- Proper Sterol Distribution Is Required forG3 (Bethesda, Md.) · 2016Article
- Neuronal deficiency of ARV1 causes an autosomal recessive epileptic encephalopathy.Human molecular genetics · 2016Article
- Deletion of murine Arv1 results in a lean phenotype with increased energy expenditure.Nutrition & diabetes · 2015Article
- Arv1; a "Mover and Shaker" of Subcellular Lipids.Contact (Thousand Oaks (Ventura County, Calif.))Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The lipid transporter Arv1 regulates sterol trafficking, and glycosylphosphatidylinositol and sphingolipid biosyntheses in Saccharomyces cerevisiae. ScArv1 contains an Arv1 homology domain (AHD) that is conserved at the amino acid level in the pathogenic fungal species, Candida albicans and Candida glabrata. Here we show S. cerevisiae cells lacking Arv1 are highly susceptible to antifungal drugs. In the presence of drug, Scarv1 cells are unable to induce ERG gene expression, have an altered pleiotrophic drug response, and are defective in multi-drug resistance efflux pump expression. All phenotypes are remediated by ectopic expression of CaARV1 or CgARV1. The AHDs of these pathogenic fungi are required for specific drug tolerance, demonstrating conservation of function. In order to understand how Arv1 regulates antifungal susceptibility, we examined sterol trafficking. CaARV1/CgARV1 expression suppressed the sterol trafficking defect of Scarv1 cells. Finally, we show that C. albicansarv1/arv1 cells are avirulent using a BALB/c disseminated mouse model. We suggest that overall cell survival in response to antifungal treatment requires the lipid transporter function of Arv1.
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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.