We are investigating the mechanisms by which non-pathogenic microbes are able to colonize, multiply, and thrive inside plant leaves.
There are two main projects in the lab:
Understanding the mechanisms behind non-pathogenic microbiota survival and multiplication inside plants.
Arabidopsis plants colonized by the microbiota strain Pandoraea sp. Col-0-28. Non-pathogenic microbes inside plants are in population stasis caused by equilibrium between the rates of multiplication and death.
Treating plants colonized with Pandoraea with an antibiotic (cefotaxime) that only targets dividing bacteria indicates that there are two sub-populations inside plants (i.e., phenotypic heterogeneity is present in the bacterial clonal population): One actively dividing, and one in true stasis.
Phenotypic heterogeneity is confirmed by using a fluorescent division reporter (promoters [P], terminators [ter], and a regulatory gene [tetR] also shown), in which dilution of the inducible signal (yellow fluorescence; expression induced with anhydrotetracycline [aTc] before colonization) indicates dividing colonies.
Are virulent pathogens experiencing Effector-triggered immunity physiologically analogous to non-pathogenic microbiota?
Recognition of Pst effector AvrPto by certain Arabidopsis accessions (e.g., Bu-22) causes Effector-triggered immunity (ETI; via Resistance protein RPS7) and prevents disease-symptom formation in plants. Pst ∆avrPto is a bacterial strain lacking avrPto that can cause disease in Bu-22 plants.
In interactions that cause ETI, in planta bacterial populations remain static after an initial increase, rendering virulent pathogenic microbes into a non-pathogenic state.
By identifying the mechanisms behind bacterial survival and multiplication, we aim to use the knowledge to develop strategies to enhance colonization by beneficial microbiota strains and hamper colonization by pathogens, thereby increasing crop productivity.