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Merfa, M. V.

Publications and source records attributed to Merfa, M. V..

4 recordsLinked to original sources

Effector loss and gain drives pathogen host range at a fitness cost

Epidemic preparedness depends on tracking microbial evolution that drives shifts in ecological behaviors such as disease emergence. However, the genetic constraints for microbial host adaptation to emerge for generalist and specialist behaviors remain poorly described. Here, we show that generalist cereal pathogen Xanthomonas translucens arose from a specialist ancestor via the loss of a single effector gene, xopAL1. Deleting barley-specialist X. translucens xopAL1 recapitulated the host jump to wheat and demonstrates risk across each globally distributed genetic lineage. However, this niche expansion via XopAL1 loss incurs a significant pathogenic fitness cost to colonize barley. Moreover, the specialist lineage gained an additional effector gene, xopAJ, which enhanced virulence on barley while restricting oat infection, thereby reinforcing niche specialization. We further identified key host pathways mediating resistance to the specialist lineage of X. translucens, opening avenues for potentially identifying targets for crop improvement. Our work provides an experimentally validated evolutionary framework to understand mechanisms of intergenera host jump. Overall, we demonstrate that single events of gene loss and gain shape ecological behaviors of pathogens by creating a dynamic trade-off between niche breadth and specialization.

microbiology↗

rpfF is not required for X. translucens pv. undulosa pathogenesis

Bacterial cells self-coordinate via a mechanism called quorum sensing. In Xanthomonas species the gene rpfF encodes the quorum sensing autoinducer synthase. Xanthomonas species are divided into two main phylogenetic groups called Clade I and Clade II. The rpf quorum sensing system has been well studied in multiple Clade II Xanthomonas species and deletion of rpfF resulted in a major loss of virulence on susceptible hosts. However, the only Clade I Xanthomonas species in which the rpfF system was previously studied was in the sugarcane pathogen X. albilineans. In X. albilineans the rpf cluster plays a relatively small role in pathogenesis. Xanthomonas translucens pv. undulosa (Xtu) is a Clade I Xanthomonas species that causes bacterial leaf streak (BLS) and black chaff of wheat and barley and has increased as a concern in recent decades. Neither major resistance nor chemical treatments are available to prevent disease caused by Xtu. Interference with rpf bacterial quorum sensing systems has demonstrated some success in other systems. It was unknown whether BLS caused by Xtu could be prevented via quorum sensing interference. We found that Xtu encodes an rpfF homolog and we created an rpfF knockout mutant to study the role of the rpf system in Xtu. We found that the rpfF mutant was unaffected in its pathogenesis as it caused BLS symptoms and multiplied within wheat plants to the same levels as the wildtype strain. The Xtu rpfF mutant grew normally in lag and log phases in vitro, however it exhibited a shorter stationary phase and an early death phase in plant-derived media. The importance of RpfF in Xtus life cycle is unknown, though it appears to carry out a role in population stability. Our research determined that rpfF is not a major Xtu pathogenicity factor. Therefore, we do not recommend the targeting of the rpf quorum sensing system as a preventative treatment for BLS of wheat.

molecular biology↗

Complete functional analysis of type IV pilus components of a reemergent plant pathogen reveals neofunctionalization of paralog genes

Type IV pilus (TFP) is a multifunctional bacterial structure involved in twitching motility, adhesion, biofilm formation, as well as natural competence. Here, by mutagenesis and functional analysis, we dissected the roles of all genes required for TFP biosynthesis and regulation in the reemergent plant pathogenic fastidious prokaryote Xylella fastidiosa. This xylem-limited, insect-transmitted pathogen lives constantly under flow conditions and therefore is highly dependent on TFP for host colonization. In addition, TFP-mediated natural transformation is a process that impacts genomic diversity and environmental fitness. Ten out of the thirty-eight genes analyzed were essential for movement and natural competence. Interestingly, seven sets of paralogs exist, and mutations showed opposing phenotypes, indicating evolutionary neofunctionalization of subunits within TFP. The minor pilin FimT3 was the only protein exclusively required for natural competence. We determined that FimT3 (but not the other two FimT paralogs) is a DNA receptor that is conserved among X. fastidiosa strains and binds DNA non-specifically via an electropositive surface. Among plant pathogens, this gene was also found in the genome of strains of the plant associated Xanthomonadaceae family. Overall, we highlight here the complex regulation of TFP in X. fastidiosa, providing a blueprint to understand TFP in other bacteria living under flow conditions.

microbiology↗

Repeated gain and loss of a single gene modulates the evolution of vascular pathogen lifestyles

Vascular pathogens travel long distances through host veins leading to life-threatening, systemic infections. In contrast, non-vascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and non-vascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and non-vascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the Xanthomonadaceae family and absent in most non-vascular species. CbsA expression allowed non-vascular Xanthomonas to cause vascular blight while cbsA mutagenesis resulted in reduction of vascular or enhanced non-vascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple non-vascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits.

microbiology↗