Our current work integrates molecular genetics and pathology, genomics and bioinformatics to gain knowledge in the field of the plant-pathogen interactions.
Broadly, our research is critical for the development of environmentally sound methods to minimize not only the impact of diseases and economic losses in agriculture worldwide, but also food contamination by human pathogens. Research in the lab is focused on two main objectives:
1) to understand the mechanisms by which plants defend themselves against bacterial infection (plant innate immunity).2) to study virulence strategies evolved by bacterial pathogens to overcome/avoid plant defenses (bacterial pathogenesis and fitness).
Basal immunity in plants, much like innate immunity in animals, is activated by the recognition of pathogen-associated molecular patterns (PAMPs; the conserved molecules among microbes). The functional role of basal innate immunity in limiting bacterial infection has been unclear until recently. We have found that a major function of the PAMP-induced innate immunity is stomatal defense against bacterial entry into the plant tissue. Opening and closure of stomata is controlled by environmental factors such as light, humidity, and CO2 concentration among others.
It has been thought that stomata (unwittingly) provide ports for bacterial entry into internal tissues. Surprisingly, we discovered that stomata function as an active defense, closing in response to plant and human pathogenic bacteria, as well as purified PAMPs. Stomatal closure in response to these treatments requires several components of the plant innate immunity and abscisic acid signaling. Thus, stomata play a crucial role in restricting bacterial infection.
We also discovered that plant pathogens are able to overcome stomatal defenses by re-opening the pore, thereby gaining entry to the intercellular spaces, ultimately leading to colonization and disease. This observation led us to hypothesize that to be a successful plant pathogen, a bacterium must evolve virulence factors to overcome stomatal defense and/or rely on environmental conditions under which stomata cannot effectively respond to PAMPs. In the case of Pseudomonas syringae pv. tomato (Pst) DC3000, which infects Arabidopsis and tomato, We have shown that the toxin coronatine is responsible for re-opening of stomata. More recently in my laboratory, we have proposed that some human pathogens could potentially trigger a weak immunity (stomatal and apoplastic) by evolving PAMPs that can no longer be recognized by plants. As an example, we have shown that Samonella enterica serovar Typhimurium SL1344, unlike Escherichia coli O157:H7, induces a mild immunity in Arabidopsis and lettuce. We provided evidence that SL1344, by avoiding plant’s recognition, may be able to penetrate and survive as an endophyte more efficiently than O157:H7.
Our current research effort is geared towards uncovering this novel and crucial early host-bacterium interaction in the phyllosphere. The discovery of host-bacterium battles at stomata represents a significant conceptual advance in our understanding of not only bacterial pathogenesis and stomatal biology but also microbial ecology of plant and human pathogenic bacteria in the phyllosphere.
Research in the lab is funded by the NIH - National Institute of Allergy and Infections Disease , UTA start up funds, as well as scholarships from the Brazilian Funding Agencies CAPES and FAPESP.