RESUMEN
The microbiome is the collection of microbes that are associated with a host. Microsporidia are intracellular eukaryotic parasites that can infect most types of animals. In the last decade, there has been much progress to define the relationship between microsporidia and the microbiome. In this review, we cover an increasing number of reports suggesting that microsporidia are common components of the microbiome in both invertebrates and vertebrates. These microsporidia infections can range from mutualistic to pathogenic, causing several physiological phenotypes, including death. Infection with microsporidia often causes a disruption in the normal microbiome, with both increases and decreases of bacterial, fungal, viral, and protozoan species being observed. This impact on the microbiome can occur through upregulation and downregulation of innate immunity as well as morphological changes to tissues that impact interactions with these microbes. Other microbes, particularly bacteria, can inhibit microsporidia and have been exploited to control microsporidia infections. These bacteria can function through regulating immunity, secreting anti-microsporidia compounds, and, in engineered versions, expressing double-stranded RNA targeting microsporidia genes. We end this review by discussing potential future directions to further understand the complex interactions between microsporidia and the other members of the microbiome.
RESUMEN
The emergence of new pathogens is an ongoing threat to human health and agriculture. While zoonotic spillovers received considerable attention, the emergence of crop diseases is less well studied. Here, we identify genomic factors associated with the emergence of Pseudomonas syringae bacterial blight of coffee. Fifty-three P. syringae strains from diseased Brazilian coffee plants were sequenced. Comparative and evolutionary analyses were used to identify loci associated with coffee blight. Growth and symptomology assays were performed to validate the findings. Coffee isolates clustered in three lineages, including primary phylogroups PG3 and PG4, and secondary phylogroup PG11. Genome-wide association study of the primary PG strains identified 37 loci, including five effectors, most of which were encoded on a plasmid unique to the PG3 and PG4 coffee strains. Evolutionary analyses support the emergence of coffee blight in PG4 when the coffee-associated plasmid and associated effectors derived from a divergent plasmid carried by strains associated with other hosts. This plasmid was only recently transferred into PG3. Natural diversity and CRISPR-Cas9 plasmid curing were used to show that strains with the coffee-associated plasmid grow to higher densities and cause more severe disease symptoms in coffee. This work identifies possible evolutionary mechanisms underlying the emergence of a new lineage of coffee pathogens.
