Macroscopic similarities cloak microscopic differences in bacterial – host interactions

It’s plainly clear that sick hosts are fundamentally altered by infection and disease progression. However, it remains unknown how changes to the host create new and preferred niches for organisms beyond the infecting pathogen and influence bacterial dynamics as phytopathogenic bacteria arrive on a leaf as immigrants and then eventually establish themselves in the apoplast which they use as an infection court or encounter established populations. We study the single host, tomato, and dual pathosystems, bacterial spot caused by Xanthomonas gardneri and bacterial speck caused by Pseudomonas syringae pv. tomato. These phytopathogens lack cell wall degrading enzymes and abandon the leaf surface and enter the leaf interior via stomata prior to initiating infection. Although macroscopic symptoms are similar between these two pathogens, we found the timing of symptom development and microscopic differences in host physiology are pathogen-dependent. Furthermore these differences affect immigrants to the infected apoplast.

Fundamental changes to infection courts by pathogens create novel niches for other microbes.

 Although the primary purpose of altering the plant environment during infection is likely for the benefit of the pathogen, sweeping changes in physical and biochemical characteristics of the host undoubtedly also reshape the composition of the bacterial community in an infection court. We have found that the dramatic change to the apoplast as a result of X. gardneri infection creates an available and habitable niche for bacteria that are usually precluded from stomatal entry and exiled to the leaf surface, such as S. enterica.

Expanding our investigation of how leaf infection changes the host, we examined whether bacteria that create water congested apoplast during infection, in general, permit leaf surface bacteria entry to this altered niche. We recently discovered that P. syringae pv tomato infection failed to permit S. enterica entry to the apoplast but most surprising, a subsequent immigration population of P. syringae pv tomato could also not join the infecting population established in the apoplast. In contrast, immigrating X. gardneri cells successfully incorporate into an established X. gardneri apoplast infection. These results support two possible outcomes that we plan to investigate: 1) changes to the apoplast of a P. syringae-infected plant results in a different carrying capacity or temporal difference than one of a X. gardneri-infected plant and/or 2) changes to the apoplast of a X. gardneri-infected plant can host a variety of bacteria from the leaf surface whereas the apoplast of a P. syringae-infected plant is limited to supporting the infecting population.

(Dr. Vicky Lason Harrod, Megan Dixon, Ellie Guilemette, Soniz Zaacks, Dr. Jeri Barak, Dr. Kim Cowles, and Natalie Wieber)