Research
When a bacterium encounters a new host, what determines whether it successfully colonizes? In the Karasov lab we aim determine the major factors limiting bacterial adaptation to new hosts.
Do bacteriophages (the viruses of bacteria) affect how bacteria evolve to colonize hosts?
Phages (viruses of bacteria) can reshape animal and plant microbial communities and can be repurposed to prevent pathogen spread (e.g. phage therapy). Wild plant populations are relatively resistant to pathogenic outbreaks. Whether phages help to protect wild plant populations from pathogenic outbreaks is unknown. We are currently characterizing the phage and their related genetic elements that infect A. thaliana microbiomes to determine (i) host specificity and abundance of phyllosphere-associated phages and (ii) the temporal evolution of bacterial and phage genotypes using modern and historical samples. This work incorporates metagenomics of historical and modern microbiomes with functional testing of phage host preferences. The synthesis of ancient and modern metagenomics, microbiology and plant pathology will reveal how phages influence the evolution of a prominent plant pathogen and contribute to the control of disease spread in plant populations.
For a pathogen that can infect both plant and animal hosts, does the pathogen infect the disparate hosts using the same mechanisms or divergent mechanisms?
While it is clear that bacterial pathogens often infect only a subset of available host species, we rarely know the genetic mechanisms that prevent them from making a host jump to colonize new hosts. To address this gap in our knowledge, this research project determines the host genetic that limit bacterial adaptation to new hosts. The results of this research will inform our understanding of the barriers that prevent a bacterium from colonizing a new host and will improve our ability to predict microbial host jumps.
Are plant metabolites important for suppressing bacterial growth in plant populations?
Plant-associated pathogens have evolved to infect specific hosts, and in turn, plant species have evolved to resist specific pathogens. One layer of plant defense against pests is the production of metabolites. We are interested in understanding how plant pathogens adapt in the presence of these metabolites. Focusing on plants from the family Brassicaceae (the mustards) and the glucosinolate compounds, we are determining whether bacteria (i) have adapted to the metabolites of their hosts (ii) the mechanisms of adaptation to abundant metabolites. To understand the importance of specialized metabolites in plant-pathogen interactions, we are using a combination of functional genomics and biochemical assays to characterize genome wide which specialized metabolites are involved in interactions, and which influence microbial host preferences.
In aspen populations of the Mountain West, how does drought influence pathogen spread?
Drought in Aspen results in a range of physiological changes both contemporaneous with the drought event and in the subsequent seasons. The aim of this project is to determine how drought exposure influences the trees’ immune system and susceptibility to microbial disease. In parallel with the Anderegg’s large-scale common garden and wild drought experiments, we are assaying markers of immune induction and pathogen abundance. We are assaying (i) the induction of defense chemicals (metabolomics) (ii) the induction of immune-related genes (qPCR and RNA-seq) and (iii) the abundance of fungal and bacterial microbiota (16S rRNA sequencing, ITS sequencing). Combining this information with plant physiolgical measurements made by the Anderegg lab we will draw associations between drought exposure, plant physiological stress and the trees’ immune function.
