Abstract
Cyclic 3′,5′-adenosine monophosphate (cAMP) is a nucleotide derived from adenosine triphosphate that acts as a second messenger throughout all kingdoms. Intracellular cAMP levels are synthesized by a membrane-bound protein, the adenylyl cyclase. In order to analyze the function of this gene and the importance of cAMP in the life cycle of the cereal pathogen Fusarium graminearum, the adenylyl cyclase gene (FGSG_01234) was deleted by gene replacement (ΔFgac1). The ΔFgac1 mutant displayed a drastically reduced growth on agar medium which could be rescued by a cAMP analogon. Furthermore, the ΔFgac1 mutant was unable to produce perithecia on detached wheat nodes. However, artificial conditions like carrot agar allowed perithecia development. Pathogenicity towards wheat was drastically reduced in ΔFgac1 compared to the wild type. Point-inoculated spikelets showed only small lesions but no typical head blight disease symptoms. Fluorescence microscopy using dsRed-expressing strains revealed that the ΔFgac1 strain was unable to develop any complex infection structures like lobate appressoria and infection cushions. Instead, hyphal anastomosis occurs frequently. Scanning electron microscopy demonstrated the lack of fungal penetration. Hence, the formation of compound appressoria seems to be essential for infection of wheat. Hyphae on flower leaves produced huge amounts of new conidia, thereby circumventing the infection cycle. This abundant sporulation on wheat epidermis was not observed in wild type. Intriguingly, the Fgac1 deletion mutant was able to infect maize cobs as wild type, indicating that cAMP signaling is not important for maize infection. The ΔFgac1 mutant was unable to produce the mycotoxin deoxynivalenol both in vitro and during wheat infection. In this study, we show that cAMP signaling controls important cellular processes such as development of infection structures, pathogenicity, secondary metabolite production and sexual reproduction. For the first time, we show that cAMP regulates the switch from vegetative to pathogenic lifestyle of F. graminearum on wheat.
Highlights
Fusarium graminearum is the main causal agent of Fusarium head blight (FHB) disease of small grain cereals like wheat (Triticum aestivum) and barley (Hordeum vulgare) and of ear rot of maize
The in-vitro DON measurements were normalized to the fungal dry mass, while the in-planta DON measurements were normalized to the amount of fungal biomass using qPCR as described previously [30]. These results demonstrate that DON biosynthesis in culture as well as during wheat infection depends on cAMP signaling
The entire life cycle of F. graminearum in nature relies on the successful colonization of a susceptible host plant by its infecting agents, i.e. macroconidia and ascospores
Summary
Fusarium graminearum is the main causal agent of Fusarium head blight (FHB) disease of small grain cereals like wheat (Triticum aestivum) and barley (Hordeum vulgare) and of ear rot of maize. Full virulence on wheat relies on the production of the highly toxic trichothecene deoxynivalenol (DON). It is synthesized by the fungus in high amounts during infection and post harvest. For the initial penetration, DON biosynthesis is dispensable, its biosynthesis is enhanced during formation of compound appressoria on the surface of wheat floral organs [1]. This raises the question which signals trigger the mycotoxin biosynthesis and the development of infection structures and how these signals are perceived
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