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Zaacks, S. C.

Publications and source records attributed to Zaacks, S. C..

3 recordsLinked to original sources

Established Pseudomonas syringae pv. tomato infection disrupts immigration of leaf surface bacteria to the apoplast

Bacterial disease alters the infection court creating new niches. The apoplast is an oasis from the hardships of the leaf surface and is generally inaccessible to nonpathogenic members of the phyllosphere bacterial community. Previously, we demonstrated that Salmonella enterica immigrants to the leaf surface can both enter the apoplast and replicate due to conditions created by an established Xanthomonas hortorum pv. gardneri (Xhg) infection. Here, we have expanded our investigation of how infection changes the host by examining the effects of another water-soaking pathogen, Pseudomonas syringae pv tomato (Pst), on immigrating bacteria. We discovered that, despite causing macroscopically similar symptoms as Xhg, Pst infection disrupts S. enterica colonization of the apoplast. To determine if these effects were broadly applicable to phyllosphere bacteria, we examined the fates of immigrant Xhg and Pst arriving on an infected leaf. We found that this effect is not specific to S. enterica, but that immigrating Xhg or Pst also struggled to fully join the infecting Pst population established in the apoplast. To identify the mechanisms underlying these results, we quantified macroscopic infection symptoms, examined stomata as a pinch point of bacterial entry, and characterized aspects of interbacterial competition. While it may be considered common knowledge that hosts are fundamentally altered following infection, the mechanisms that drive these changes remain poorly understood. Here, we investigated these pathogens to reach a deeper understanding of how infection alters a host from a rarely accessible, inhabitable environment to an obtainable, habitable niche. IMPORTANCEPathogens dramatically alter the host during infection. Changes in host physical and biochemical characteristics benefit the pathogen and can reshape the composition of the bacterial community. In fact, rare members of the plant microbiota, namely bacterial human pathogens, such as Salmonella enterica, thrive in some plant infection courts. The increased success of human pathogens results from the conversion of the rarely accessible, inhabitable apoplast to an obtainable, habitable niche following infection. Here, we compared two phytopathogens, Pseudomonas syringae pv. tomato and Xanthomonas hortorum pv. gardneri within a tomato host and uncovered relevant niche changes potentially overlooked by the similarity in macroscopic symptoms. We investigated mechanisms used to reshape the host environment to the pathogens benefit and either success or failure of newly arriving immigrant bacteria. This study reveals information about bacterial disease of leaves and key changes that remodel inhospitable niches to new, conducive environments in the diseased host.

microbiology↗

Time of arrival during disease progression and humidity additively influence Salmonella enterica colonization of lettuce

The interplay between plant host, phytopathogenic bacteria, and enteric human pathogens in the phyllosphere have consequences for human health. Salmonella enterica has been known to take advantage of phytobacterial infection to increase its success on plants, but there is little knowledge of additional factors that may influence the relationship between enteric pathogen and plant disease. In this study, we investigated the role of humidity and the extent of plant disease progression on S. enterica colonization of plants. We found that high humidity was necessary for replication of S. enterica on diseased lettuce, but not required for S. enterica ingress into the UV-protected apoplast. Additionally, the Xanthomonas hortorum pv. vitians (hereafter, X. vitians) - infected lettuce host was found to be a relatively hostile environment for S. enterica when it arrived prior to the development of watersoaking or following necrosis onset, supporting the existence of an ideal window during X. vitians infection progress that maximizes S. enterica survival. In vitro growth studies in sucrose media suggest that X. vitians may allow S. enterica to benefit from cross-feeding during plant infection. Overall, this study emphasizes the role of phytobacterial disease as a driver of S. enterica success in the phyllosphere, demonstrates how time of arrival during disease progress can influence S. entericas fate in the apoplast, and highlights the potential for humidity to transform an infected apoplast into a growth-promoting environment for bacterial colonizers. ImportanceBacterial leaf spot of lettuce caused by X. vitians is a common threat to leafy green production. The global impact caused by phytopathogens, including X. vitians, is likely to increase with climate change. We found that even under a scenario where increased humidity did not enhance plant disease, high humidity had a substantial effect on facilitating S. enterica growth on Xanthomonas-infected plants. High humidity climates may directly contribute to the survival of human enteric pathogens in crop fields or indirectly affect bacterial survival via changes to the phyllosphere brought on by phytopathogen disease.

microbiology↗

Xanthomonas infection transforms the apoplast into an accessible and habitable niche for Salmonella enterica

The physiology of plant hosts can be dramatically altered by phytopathogens. Xanthomonas hortorum pv. gardneri is one such pathogen that creates an aqueous niche within the leaf apoplast by manipulating the plant via the transcription activator-like effector AvrHah1. Simultaneous immigration of X. gardneri and Salmonella enterica to healthy tomato leaves results in increased survival of S. enterica as Xanthomonas infection progresses. However, the fate of S. enterica following arrival on actively infected leaves has not been examined. We hypothesized that the water-soaking caused by X. gardneri could facilitate the ingression of S. enterica into the apoplast, and that this environment would be conducive for growth. We found that a water-soaked apoplast, abiotically or Xanthomonas-infected, enabled surface S. enterica to passively localize to the protective apoplast and facilitated migration of S. enterica to distal sites within the aqueous apoplast. AvrHah1 contributed to the protection and migration of S. enterica early in X. gardneri infection. Xanthomonas-infected apoplasts facilitated prolonged survival and promoted S. enterica replication compared to healthy apoplasts. Access to an aqueous apoplast in general protects S. enterica from immediate exposure to irradiation whereas, the altered environment created by Xanthomonas infection provides growth-conducive conditions for S. enterica. Overall, we have characterized an ecological relationship in which host infection converts an unreachable niche to a habitable environment. ImportanceBacterial spot disease caused by Xanthomonas species devastates tomato production worldwide. Salmonellosis outbreaks from consumption of raw produce have been linked to the arrival of Salmonella enterica on crop plants in the field via contaminated irrigation water. Considering that Xanthomonas is difficult to eradicate, it is highly likely that S. enterica arrives on leaves pre-colonized by Xanthomonas with infection underway. Our study demonstrates that infection and disease fundamentally alter the leaf, resulting in redistribution and change in abundance of a phyllosphere bacterial member. These findings contribute to our understanding of how S. enterica manages to persist on leaf tissue despite lacking the ability to liberate nutrients from plant cells. More broadly, this study reveals a mechanism by which physiochemical changes to a host environment imposed by a plant pathogen can convert an uninhabitable leaf environment into a hospitable niche for select epiphytic microbes.

microbiology↗