Abstract
An enduring theme in pathogenic microbiology is poor understanding of the mechanisms of host specificity. Metarhizium is a cosmopolitan genus of invertebrate pathogens that contains generalist species with broad host ranges such as M. robertsii (formerly known as M. anisopliae var. anisopliae) as well as specialists such as the acridid-specific grasshopper pathogen M. acridum. During growth on caterpillar (Manduca sexta) cuticle, M. robertsii up-regulates a gene (Mest1) that is absent in M. acridum and most other fungi. Disrupting M. robertsii Mest1 reduced virulence and overexpression increased virulence to caterpillars (Galleria mellonella and M. sexta), while virulence to grasshoppers (Melanoplus femurrubrum) was unaffected. When Mest1 was transferred to M. acridum under control of its native M. robertsii promoter, the transformants killed and colonized caterpillars in a similar fashion to M. robertsii. MEST1 localized exclusively to lipid droplets in M. robertsii conidia and infection structures was up-regulated during nutrient deprivation and had esterase activity against lipids with short chain fatty acids. The mobilization of stored lipids was delayed in the Mest1 disruptant mutant. Overall, our results suggest that expression of Mest1 allows rapid hydrolysis of stored lipids, and promotes germination and infection structure formation by M. robertsii during nutrient deprivation and invasion, while Mest1 expression in M. acridum broadens its host range by bypassing the regulatory signals found on natural hosts that trigger the mobilization of endogenous nutrient reserves. This study suggests that speciation in an insect pathogen could potentially be driven by host shifts resulting from changes in a single gene.
Highlights
An enduring theme in pathogenic microbiology is poor understanding of the mechanisms of host specificity
What factors limit a pathogens host range, how is host specificity linked with virulence and what changes in pathogens or hosts can open new host ranges? These are fundamental questions that relate both to the co-evolution of host susceptibility and pathogen virulence, as well as to factors underlying host switching and the emergence of new pathogens that originate in different host species
In this paper we describe molecular mechanisms controlling the host selectivity of M. robertsii strain M. robertsii such as ARSEF2575 (Mr2575), a generalist able to infect hundreds of insect species, and M. acridum strain M. acridum ARSEF324 (Ma324), a specialist pathogen of grasshoppers and locusts
Summary
An enduring theme in pathogenic microbiology is poor understanding of the mechanisms of host specificity. A number of plant pathogenic fungi produce secondary metabolites with biological specificities that correspond with the host range of the producing fungi [1,2], and small secreted proteins produced by the pathogen can trigger resistance in some plants limiting host range [3]. To date these have not been found in animal pathogenic fungi, many of which seem to be broadly opportunistic. In contrast to the opportunistic pathogens, many of these have evolved narrow host ranges by as yet unknown mechanisms
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