ArticleMarine drugs2015
Activation of the silent secondary metabolite production by introducing neomycin-resistance in a marine-derived Penicillium purpurogenum G59.
Article in Marine drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Chemical Constituents of Taxodium mucronatum (Cupressaceae) and Some of Its Endophytic Fungi, and Their In Silico and In Vitro Evaluations as SARS-CoV-2 Inhibitors and as Cytotoxic Agents.Chemistry & biodiversity · 2026Article
- Advances on anticancer fungal metabolites: sources, chemical and biological activities in the last decade (2012-2023).Natural products and bioprospecting · 2024Article
- Secondary metabolites and their bioactivities fromFrontiers in microbiology · 2024Article
- Article
- Rare Chromone Derivatives from the Marine-DerivedMarine drugs · 2021Article
- Marine-DerivedMarine drugs · 2020Article
- The Structural Diversity of Marine Microbial Secondary Metabolites Based on Co-Culture Strategy: 2009-2019.Marine drugs · 2020Review
- The Application of Ribosome Engineering to Natural Product Discovery and Yield Improvement inAntibiotics (Basel, Switzerland) · 2019Review
- Time Dependency of Chemodiversity and Biosynthetic Pathways: An LC-MS Metabolomic Study of Marine-Sourced Penicillium.Marine drugs · 2016Article
- Rare Chromones from a Fungal Mutant of the Marine-Derived Penicillium purpurogenum G59.Marine drugs · 2015Article
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6 authors.
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Abstract
Introduction of neomycin-resistance into a marine-derived, wild-type Penicillium purpurogenum G59 resulted in activation of silent biosynthetic pathways for the secondary metabolite production. Upon treatment of G59 spores with neomycin and dimethyl sulfoxide (DMSO), a total of 56 mutants were obtained by single colony isolation. The acquired resistance of mutants to neomycin was testified by the resistance test. In contrast to the G59 strain, the EtOAc extracts of 28 mutants inhibited the human cancer K562 cells, indicating that the 28 mutants have acquired the capability to produce bioactive metabolites. HPLC-photodiode array detector (PDAD)-UV and HPLC-electron spray ionization (ESI)-MS analyses further indicated that diverse secondary metabolites have been newly produced in the bioactive mutant extracts. Followed isolation and characterization demonstrated that five bioactive secondary metabolites, curvularin (1), citrinin (2), penicitrinone A (3), erythro-23-O-methylneocyclocitrinol (4) and 22E-7α-methoxy-5α, 6α-epoxyergosta-8(14),22-dien-3β-ol (5), were newly produced by a mutant, 4-30, compared to the G59 strain. All 1-5 were also not yet found in the secondary metabolites of other wild type P. purpurogenum strains. Compounds 1-5 inhibited human cancer K562, HL-60, HeLa and BGC-823 cells to varying extents. Both present bioassays and chemical investigations demonstrated that the introduction of neomycin-resistance into the marine-derived fungal G59 strain could activate silent secondary metabolite production. The present work not only extended the previous DMSO-mediated method for introducing drug-resistance in fungi both in DMSO concentrations and antibiotics, but also additionally exemplified effectiveness of this method for activating silent fungal secondary metabolites. This method could be applied to other fungal isolates to elicit their metabolic potentials to investigate secondary metabolites from silent biosynthetic pathways.
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