We are investigating the mechanisms by which non-pathogenic microbes are able to colonize, multiply, and thrive inside plant leaves.

We mainly study the interaction between Arabidopsis and Pseudomonas syringae (Pst), although we have ventured into evaluating the colonization of plants by endogenous non-pathogenic microbiota. We also use tobacco and tomato plants for our research.

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.

In planta colonization of commensal-simulating Pst ∆hrcC∆CFA at 5 days shows colonies that arose from new division (circled in magenta), and those that were static (circled in white) over the 5-day experiment.

  • 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.

We are also comparing the recognition of AvrPto in the Brassicaceae (Arabidopsis) and Solanaceae (tomato and tobacco), plant lineages that diverged over 100 million years ago.

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.