Maeli Melotto

RESEARCH OVERVIEW My research interests lie at the intersection of the disciplines of plant molecular biology, genetics, plant pathology, microbiology, and molecular plant-microbe interactions. I study the molecular mechanisms of plant (crop and model plants) immunity against pathogens and virulence strategies employed by bacteria to overcome plant defenses. Broadly, this 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. STOMATAL IMMUNITY AND BACTERIAL VIRULENCE 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. I found that a major function of the PAMP-triggered immunity (PTI) is stomatal defense against bacterial entry into the plant tissue. Stomatal opening and closure is controlled by environmental factors such as light, humidity, and CO2 concentration among others. It has been thought that because stomata open during the day for photosynthesis, they (unwittingly) provide ports for bacterial entry into leaves. I discovered that stomata function as an active defense mechanism by closing in response to plant and human pathogenic bacteria. Thus, stomata immunity plays a crucial role in restricting bacterial infection of plants. I 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, I have shown that the toxin coronatine is responsible for re-opening of stomata. More recently in my laboratory, I 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, possibly by avoiding plant s recognition, may be able to penetrate and survive as an endophyte more efficiently than O157:H7.