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Biology subjects

Karlovsky, P.

Publications and source records attributed to Karlovsky, P..

3 recordsLinked to original sources

Fusarium culmorum produces NX-2 toxin simultaneously with deoxynivalenol and 3-acetyl-deoxynivalenol or nivalenol

Fusarium culmorum is a major pathogen of grain crops. Infected plants accumulate deoxynivalenol (DON), 3-acetyl-deoxynivalenol (3-ADON), or nivalenol (NIV), which are mycotox-ins of the trichothecene B group. These toxins are also produced by F. graminearum species complex. New trichothecenes structurally similar to trichothecenes B but lacking the carbonyl group on C-8, designated NX toxins, were recently discovered in atypical isolates of F. graminearum from North America. Only these isolates and a few strains of a yet to be characterized Fusarium species from South Africa are known to produce NX-2 and other NX toxins. Here we report that among 20 F. culmorum strains isolated from maize, wheat, and oat in Europe and Asia over a period of 70 years, 18 strains produced NX-2 simultaneously with 3-ADON and DON or NIV. Rice cultures of strains producing 3-ADON accumulated NX-2 in amounts corresponding to 2-8% of 3-ADON (1.2 - 36 mg/kg). A strain producing NIV accumulated NX-2 and NIV at comparable amounts (13.6 and 10.3 mg/kg, respectively). In F. graminearum, producers of NX-2 possess a special variant of cytochrome P450 monooxygenase encoded by TRI1 that is unable to oxidize C-8. In F. culmorum, producers and non-producers of NX-2 possess identical TRI1; the reason for the production of NX-2 is unknown. Our results indicate that production of NX-2 simultaneously with trichothecenes B is a common feature of F. culmorum. Key resultIsolates of Fusarium culmorum obtained from different hosts at different locations over several dec-ades produced NX-2, which is a type A trichothecene structurally related to 3-ADON.

microbiology↗

Hülle-cell-mediated protection of fungal reproductive and overwintering structures against fungivorous animals

Fungal Hulle cells with nuclear storage and developmental backup functions are reminiscent of multipotent stem cells. In the soil, Hulle cells nurse the overwintering fruiting bodies of Aspergillus nidulans. The genome of A. nidulans harbors genes for the biosynthesis of xanthones. We show that enzymes and metabolites of this biosynthetic pathway accumulate in Hulle cells under the control of the regulatory velvet complex, which coordinates development and secondary metabolism. Deletion strains blocked in the conversion of anthraquinones to xanthones are delayed in maturation and growth of fruiting bodies. Xanthones are not required for sexual development but exert antifeedant effects on fungivorous animals such as springtails and woodlice. These findings reveal a novel role of Hulle cells in establishing secure niches for A. nidulans by accumulating metabolites with antifeedant activity that protect reproductive structures from animal predators.

biochemistry↗

Various components of the RNAi pathway are required for conidiation, ascosporogenesis, virulence, DON production and SIGS-mediated fungal inhibition by exogenous dsRNA in the Head Blight pathogen Fusarium graminearum

Gene silencing through RNA interference (RNAi) shapes many biological processes in filamentous fungi, including pathogenicity. In this study we explored the requirement of key components of fungal RNAi machinery, including DICER-like 1 and 2 (FgDCL1, FgDCL2), ARGONAUTE 1 and 2 (FgAGO1, FgAGO2), AGO-interacting protein FgQIP (QDE2-interacting protein), RecQ helicase (FgQDE3), and four RNA-dependent RNA polymerases (FgRdRP1, FgRdRP2, FgRdRP3, FgRdRP4), in the ascomycete mycotoxin-producing fungal pathogen Fusarium graminearum (Fg) for sexual and asexual multiplication, pathogenicity, and its sensitivity to double-stranded (ds)RNA. We corroborate and extend earlier findings that conidiation, ascosporogenesis and Fusarium Head Blight (FHB) symptom development require an operable RNAi machinery. The involvement of RNAi in conidiation is dependent on environmental conditions as it is detectable only under low light (< 2 {micro}mol m-2s-1). Although both DCLs and AGOs partially share their functions, the sexual ascosporogenesis is mediated primarily by FgDCL1 and FgAGO2, while FgDCL2 and FgAGO1 contribute to asexual conidia formation and germination. FgDCL1 and FgAGO2 also account for pathogenesis as their knock-out (KO) results in reduced FHB development. Apart from KO mutants{Delta} dcl2 and{Delta} ago1, mutants{Delta} rdrp2, {Delta}rdrp3, {Delta}rdrp4, {Delta}qde3 and{Delta} qip are strongly compromised for conidiation, while KO mutations in all RdPRs, QDE3 and QIP strongly affect ascosporogenesis. Analysis of trichothecenes mycotoxins in wheat kernels showed that the relative amount of deoxynivalenol (DON), calculated as [DON] per amount of fungal genomic DNA, was reduced in all spikes infected with RNAi mutants, suggesting the possibility that the fungal RNAi pathways affect Fgs DON production in wheat spikes. Moreover, gene silencing by exogenous target gene specific dsRNA (spray-induced gene silencing, SIGS) is dependent on fungal DCLs, AGOs, and QIP, but not on QDE3. Together these data show that in F. graminearum different key components of the RNAi machinery are crucial in different steps of fungal development and pathogenicity.

pathology↗