Erwinia amylovora is a highly destructive bacterial pathogen that causes fire blight disease of fruit trees, such as apple and pear. Fire blight was first reported in the Hudson Valley of New York in 1794, and it has henceforth spread to more than 50 countries across the world. In the United States, a fire blight epidemic in Michigan killed more than 400,000 apple trees in a single year, hitting the local apple industry hard. Based on a survey of the journal Molecular Plant Pathology, E. amylovora ranked as the 7th scientifically and economically most important plant pathogenic bacterium.
George Sundin of Michigan State University studies E. amylovora Fire Blight disease. This study reveals insights into the molecular processes deployed by the bacterium to successfully spread through host trees. By focussing on a small RNA molecule, his group* explored complex regulatory networks required by the bacterium to adapt to differential plant host environments.
Spreading through the host: using the Type 3 Secretion System and biofilm formation to infect the host and nourish the pathogen.
“Management of fire blight is notoriously difficult, largely due to the complexity of its pathogenesis. Fire blight infection is manifested by four stages: flower infection, shoot infection, systemic infection, and canker development. Successful infection in each stage is achieved through precise coordination of several bacterial “weapons” called virulence factors. Main virulence factors of E. amylovora include the type III secretion system (T3SS), a needle-like bacterial machinery for suppression of host immunity, flagellum-dependent motility, which allows the free movement of bacterial cells driven by lash-like appendages called flagella, and several exopolysaccharides, the extracellular carbohydrate polymers accumulating outside bacterial cells.”
Increasing biofilm formation results in spread through the xylem.
“During the shoot infection stage of fire blight, E. amylovora infects leaves at shoot tips. This infection stage is initiated in plant parenchymal cell layers through use of the T3SS, but E. amylovora cells later move to leaf veins, where they invade xylem elements and develop robust biofilms. We hypothesize that the biofilm formation stage of infection contributes to increases in population size of the pathogen in leaves, prior to further systemic movement of the pathogen from leaves into stems. Increases in population size are necessary because E. amylovora can also emerge from infected tissue in ooze droplets, that serve to disseminate the pathogen to new infection sites within the infected tree or on adjacent trees. Ooze droplets contain very large numbers of E. amylovora cells (> 1 billion cells per droplet). Thus, to be able to divert such a large number of cells to external dissemination, the internal, systemically-spreading population must be much larger.
Thus, robust biofilm development in leaf xylem is an important stage of the virulence process. However, the fire blight pathogen systemically moves through trees in the parenchymal cell layers using the T3SS, as these layers are closest to the outer surface of trees, where the pathogen needs to be located to facilitate ooze emergence and also canker formation, which is the site of overwintering. A complex set of regulatory gymnastics is required for E. amylovora cells to transition from biofilm development to T3SS-mediated pathogenesis. In our study, we report on a regulatory small RNA (sRNA) that we have found is a critical regulator in this transition.”
sRNAs – influencing gene expression
“Our recent study provided evidence for the critical modulatory roles of a small RNA (sRNA), called RprA, in orchestrating major virulence factors of E. amylovora. sRNAs are short and highly structured non-coding RNA molecules, which interact with specific messenger RNAs and modulate their translation, positively or negatively. We showed that activation of RprA promotes the transition of E. amylovora cells from a sessile to a motile lifestyle, which consequently allows the bacteria to move throughout the host. So, how do E. amylovora cells know when to turn on or off RprA production?”
RprA – an sRNA produced by E. amylovora inside the host apoplast (leaf and outer stem)
“We demonstrated that RprA production is highly induced in cells immersed in a low pH and low nutrient medium that mimics the environmental conditions encountered in the host during T3SS-mediated infection. Therefore, as the infection progresses with the host, E. amylovora cells sense environmental changes to tweak the production of RprA and potentially many other sRNAs to prime the production of individual virulence factors for its full virulence. Our study sheds light on the functions of sRNAs during systemic infection of a plant-pathogenic bacterium, which have not yet been investigated in most plant pathosystems.”
This represents a new discovery for bacterial pathogens of plants by establishing the presence of a previously unknown molecular mechanism that allows the bacterium to transition out of the biofilm phase of growth.
*Jingyu Peng, Jeffrey K. Schachterle and George W. Sundin published this study in Molecular Plant Pathology Journal. Jingyu Peng graduated with his PhD in November 2020, and is currently a Digital Native Trait Scientist at Bayer Crop Science in St. Louis, MO. Jeff Schachterle graduated with his PhD in June 2019 and is currently a postdoctoral scientist at the USDA-ARS Floral and Nursery Plants Research Unit in Beltsville, MD:
TITLE IMAGE: Young apple trees displayed shoot infection with Fireblight bacteria, Erwinia amylovora. All images used with permission of the author.
