Caitilyn Allen
VerifiedUniversity of Wisconsin-Madison · Plant Pathology
Active 1986–2026
About
Caitilyn Allen is a Professor Emeritus in the Department of Plant Pathology at the University of Wisconsin-Madison. She holds a Ph.D. from Virginia Polytechnic Institute and State University in Plant Pathology. Her research focuses on the interactions between the plant pathogenic bacterium Ralstonia solanacearum and its many plant hosts. R. solanacearum causes bacterial wilt, a soilborne disease found in tropical and warm temperate regions worldwide, and is considered one of the most harmful bacterial plant pathogens due to its broad host range and wide geographical distribution. Her work aims to identify traits that enable R. solanacearum to cause wilt disease in the nutrient-poor and microaerobic environment of the plant xylem. She studies how the bacterium uses inorganic nitrogen for pathogenesis, its mechanisms for surviving at low oxygen levels, and the role of nitric oxide in virulence. Additionally, her research investigates intrastrain competition among R. solanacearum strains, focusing on bacteriocins and their role in microbial competition and pathogen exclusion. She also explores the contribution of extracellular nucleases (NucA and NucB) to bacterial virulence, biofilm formation, and nutrient acquisition during infection. Allen's research extends to understanding the interactions between R. solanacearum and bioterrorism concerns, particularly regarding the Race 3 Biovar 2 strain, which is listed as a potential bioterrorism agent in the United States. Her work with this pathogen includes studying its interaction with geraniums and developing regulatory policies based on biological risk assessments. Throughout her career, she has contributed to the understanding of bacterial wilt disease mechanisms, microbial competition, and plant-microbe interactions.
Research topics
- Botany
- Biology
- Evolutionary biology
- Immunology
- Ecology
- Genetics
Selected publications
Proceedings of the National Academy of Sciences · 2026-01-22 · 2 citations
articleOpen accessRalstonia solanacearum species complex (RSSC) pathogens cause destructive plant wilt diseases of a wide variety of crops, leading to significant agricultural losses worldwide. These bacteria rapidly spread through the water-transporting xylem where they grow prolifically and produce abundant biofilm that clogs xylem vessels. To understand RSSC biofilm behavior in planta, we examined their complex fluid mechanics. Rheological analyses revealed that unlike all previously analyzed microbial biofilms, RSSC biofilms are shear-thinning, viscoelastic fluids at physiologically relevant shear forces. To determine which factors confer these unique mechanics, we analyzed biofilms of bacterial mutants with altered biofilm components. Genetic analysis demonstrated that development of the viscous-dominant biofilms required production of EPS-I, an amphiphilic exopolysaccharide that is a major virulence factor for all RSSC pathogens. We show that EPS-I confers “biofilm mobility”, which allows wild-type RSSC colonies to passively expand when deformed. Despite its high metabolic cost, bioassays demonstrated that EPS-I production conferred a net fitness benefit where biofilm mobility allowed the pathogen to spread and access more nutrients in complex environments like xylem vessels. The RSSC are a monophyletic lineage of aggressive plant wilt pathogens, and our evolutionary hypothesis testing suggests the origin of the eps biosynthetic gene cluster coincides with the emergence of wilt pathogenesis in the RSSC ancestor. Furthermore, comparative physiological assays demonstrated that biofilm mobility is unique to the RSSC within the genus Ralstonia . In summary, EPS-I production is a key evolutionary innovation that enables RSSC dispersal and virulence by conferring unique biofilm mechanics.
Trehalose, a Biostimulant to Reduce Bacterial Wilt Disease on Tomato
Plant Health Progress · 2025-01-01
articleSenior authorFarmers suffer large losses to bacterial wilt, a widespread crop disease caused by soilborne Ralstonia species. There is no good control for bacterial wilt, which affects many economically important crops, including tomato. Trehalose is an environmentally benign non-reducing disaccharide that is present in all kingdoms of life. Previous studies suggested that trehalose has potential as a biostimulant to reduce bacterial wilt of tomatoes and also to increase plant drought tolerance. We sought to define optimal strategies to apply this biostimulant for tomato plant protection. Imbibing seeds with a 30 mM trehalose solution before planting slightly increased drought tolerance but did not increase bacterial wilt resistance. However, exogenous application of 30 mM trehalose solutions substantially reduced wilt disease severity on tomato plants inoculated with high doses of Ralstonia pseudosolanacearum strain GMI1000. Trehalose was protective when applied either by soaking bare-root seedlings at the time of transplant or as a soil drench to older plants. Three or more trehalose soil drenches rendered tomato plants highly resistant to Ralstonia but also decreased their biomass and leaf chlorophyll content. Reducing the number of soil drenches to two resulted in good protection from bacterial wilt with minimal phytotoxicity. Soaking bare-root seedlings in trehalose also increased bacterial wilt resistance without major effects on plant health. Together, these experiments identified an environmentally sustainable solution for a common and destructive plant disease.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-22
preprintOpen accessAbstract Ralstonia solanacearum species complex (RSSC) pathogens cause destructive plant wilt diseases of a wide variety of crops, leading to significant agricultural losses worldwide. These bacteria rapidly spread through the water-transporting xylem where they grow prolifically and produce abundant biofilm that clogs xylem vessels. To understand RSSC biofilm behavior in planta , we examined their complex fluid mechanics. Rheological analyses revealed that unlike all previously analyzed microbial biofilms, RSSC biofilms are shear-thinning, viscoelastic fluids at physiologically relevant shear forces. To determine which factors confer these unique mechanics, we analyzed biofilms of bacterial mutants with altered biofilm components. Genetic analysis demonstrated that development of the viscous-dominant biofilms required production of EPS-I, an amphiphilic exopolysaccharide that is a major virulence factor for all RSSC pathogens. We show that EPS-I confers “biofilm mobility”, which allows wildtype RSSC colonies to passively expand when deformed. Despite its high metabolic cost, bioassays demonstrated that EPS-I production conferred a net fitness benefit where biofilm mobility allowed the pathogen to spread and access more nutrients in complex environments like xylem vessels. The RSSC are a monophyletic lineage of aggressive plant wilt pathogens, and our evolutionary hypothesis testing suggests the origin of the eps biosynthetic gene cluster coincides with the emergence of wilt pathogenesis in the RSSC ancestor. Furthermore, comparative physiological assays demonstrated that biofilm mobility is unique to the RSSC within the genus Ralstonia . In summary, EPS-I production is a key evolutionary innovation that enables RSSC dispersal and virulence by conferring unique biofilm mechanics. Significance Statement Ralstonia solanacearum species complex (RSSC) pathogens threaten global food security by fatally wilting plants. A soft matter physics lens demystified the cryptic role of a major virulence factor, the EPS-I exopolysaccharide. EPS-I transforms RSSC biofilms into viscoelastic fluids, a mechanical behavior not previously described for other microbial biofilms that are almost always viscoelastic solids. We demonstrate that the development of fluid biofilms was a key evolutionary innovation that enabled pathogenic success of these aggressive pathogens that rapidly wilt plants.
Phytobiomes Journal · 2025-07-29 · 1 citations
articleOpen accessSenior authorPlant-associated microbes can reduce dependance on conventional agrochemicals by enhancing plant health and productivity through the production of biomolecules. Potato growers depend on healthy seed tubers, but chemical inputs are currently needed to ensure good yields of pathogen-free seed tubers. Adding beneficial microorganisms to a plant micropropagation system offers a more sustainable way to enhance productivity. We hypothesized that introducing natural potato endophytic bacteria to plantlets in tissue culture could increase seed potato minitubers. Bacterial endophytes were isolated from field-grown potato tubers and stems, selected for ability to harmlessly bacterize (colonize) in vitro plantlets, and screened for effects on plant growth and productivity. One promising candidate, named UW852, significantly increased tuber productivity in greenhouse trials. Phylogenetic analysis of the complete UW852 genome identified it as an actinomycete in the genus Arthrobacter. The genome putatively encodes synthesis of at least one iron-sequestering siderophore and the plant growth substance gibberellic acid. In vitro assays confirmed that the UW852 culture cell-free supernatant contains both siderophore activity and lettuce hypocotyl elongation activity consistent with production of gibberellic acid. UW852 remained detectable in 70% of daughter tubers harvested from plants that had been bacterized in vitro, suggesting that this bacterium can confer beneficial effects over a growing season or longer. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .
Potato Cv. ‘Granola’ Has Moderate Tolerance for Bacterial Wilt Disease
American Journal of Potato Research · 2025-09-02
articleOpen accessSenior authorAbstract Bacterial wilt or brown rot caused by Ralstonia solanacearum is among the most destructive diseases of potato in tropical highlands worldwide. There are no completely wilt-resistant varieties, but growers can reduce losses by planting partially resistant or tolerant potatoes. We screened the popular tropical potato cv. ‘Granola’ for bacterial wilt resistance under controlled conditions. Granola plants inoculated with high doses of R. solanacearum IIB-1 (Race 3 biovar 2) had reduced wilt disease progress relative to susceptible control cv. ‘Russet Norkotah’. Although the pathogen did colonize Granola plants, it reached significantly lower population sizes in Granola stems, stolons, and especially tubers than in those of Russet Norkotah. These results suggest that Granola has some tolerance to bacterial wilt, likely mediated by suppression of bacterial colonization. Thus, Granola could be a useful parent for tropical potato breeding programs.
mBio · 2025-12-08 · 1 citations
articleOpen accessSenior authorABSTRACT Ralstonia pseudosolanacearum ( Rp s), which causes bacterial wilt disease of many crops, must integrate environmental signals to successfully transition from soil to its pathogenic niche in host plant xylem tissue. Mutating a gene encoding a putative sensing/signaling protein had little transcriptomic effect on Rps strain GMI1000 in culture. However, when the mutant grew in tomato, over 180 genes were differentially expressed relative to the wild type. The gene was therefore named rprR for R alstonia p lant- r esponsive r egulator. In planta , the ∆ rprR mutant dysregulated genes for diverse traits, including stress response, degradation of phenolic compounds, motility, attachment, and production of extracellular polysaccharide (EPS), which is a key bacterial wilt virulence factor. Quantifying Rps EPS by ELISA found increased levels in stems of plants infected with ∆ rprR as compared to the wild type. Functional assays showed that ∆ rprR is defective in attachment to tomato roots, colonization of tomato stems, and bacterial wilt virulence. In a rich medium, ∆ rprR formed biofilm normally, but the mutant formed less biofilm in tomato stem homogenate and in tomato xylem sap under flow. This phenotype correlates with the mutant’s altered expression of EPS biosynthetic genes and aberrant extracellular matrix. When grown in tomato stem homogenate, ∆ rprR produced 57% more of the bacterial signal cyclic di-GMP (c-di-GMP) than the wild type. This is consistent with the presence, in RprR, of predicted c-di-GMP-modulating domains. Together, these findings reveal that RprR, which is highly conserved across plant pathogenic Ralstonia , modulates several bacterial wilt virulence traits in response to the plant host. IMPORTANCE Members of the Ralstonia solanacearum species complex (RSSC) cause bacterial wilt, a globally destructive disease of market and subsistence crops. Like other plant-associated microbes, bacteria in the RSSC must integrate a complex array of biotic and abiotic signals to successfully infect plant hosts. All RSSC genomes encode an unusual protein, termed RprR, that contains multiple sensing and signaling domains, including two putative modulators of the secondary messenger c-di-GMP. Deleting RprR in Ralstonia pseudosolanacearum affected many virulence properties, including production of biofilm and exopolysaccharide, and increased intracellular c-di-GMP levels, all in a strictly plant-dependent fashion. While c-di-GMP has been investigated in other plant pathogenic bacteria, this is the first report of its role in the RSSC. Most importantly, rprR was required for Ralstonia to effectively colonize plants and cause wilt disease. Thus, RprR is a plant-responsive sensor-regulator that controls pathogen adaptation to the host environment and virulence.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-12
preprintOpen accessSenior authorCorrespondingAbstract Ralstonia pseudosolanacearum ( Rp s), which causes bacterial wilt disease of many crops, must integrate environmental signals to successfully transition from soil to its pathogenic niche in host plant xylem tissue. Mutating a putative sensing/signaling gene had little transcriptomic effect on Rps strain GMI1000 in culture. However, when the mutant grew in tomato over 180 genes were differentially expressed relative to wild type. The gene was therefore named rprR for R alstonia p lant-responsive regulator. In planta , the Δ rprR mutant dysregulated genes for diverse traits including stress response, degradation of phenolic compounds, motility, attachment, and production of extracellular polysaccharide (EPS), which is a key bacterial wilt virulence factor. Quantifying Rps EPS by ELISA found increased levels in stems of plants infected with Δ rprR as compared to wild type. Functional assays showed Δ rprR is defective in attachment to tomato roots, colonization of tomato stems, and bacterial wilt virulence. In rich medium, Δ rprR formed biofilm normally, but the mutant formed less biofilm in tomato stem homogenate and in tomato xylem sap under flow. This phenotype correlates with the mutant’s altered expression of EPS biosynthetic genes and aberrant extracellular matrix. When grown in tomato stem homogenate, Δ rprR produced 57% more of the bacterial signal cyclic di-GMP (c-di-GMP) than wild type. This is consistent with the presence in RprR of predicted c-di-GMP modulating domains. Together these findings reveal that RprR, which is highly conserved across plant pathogenic Ralstonia , modulates several bacterial wilt virulence traits in response to the plant host. Importance Members of the Ralstonia solanacearum species complex (RSSC) cause bacterial wilt, a globally destructive disease of market and subsistence crops. Like other plant-associated microbes, bacteria in the RSSC must integrate a complex array of biotic and abiotic signals to successfully infect plant hosts. RSSC genomes all encode an unusual protein, termed RprR, that contains multiple sensing and signaling domains, including two putative modulators of the secondary messenger c-di-GMP. Deleting RprR in Ralstonia pseudosolanacearum had a plant-dependent effect on many traits, including production of the key virulence factors biofilm and exopolysaccharide, as well as intracellular c-di-GMP levels. While c-di-GMP has been investigated in other plant pathogenic bacteria, this is the first report of its role in the RSSC. Most importantly, rprR was required for Ralstonia to effectively colonize plants and cause wilt disease. Thus, RprR is a plant-responsive sensor-regulator that controls pathogen adaptation to the host environment and virulence.
Heat Treatment to Eradicate <i>Ralstonia solanacearum</i> R3bv2 from Plant Growth Media
Plant Health Progress · 2025-01-01 · 2 citations
articleSenior authorThe pathogenic bacterium Ralstonia solanacearum race 3 biovar 2 (R3bv2) is highly regulated because it can threaten potato production. R3bv2 can also infect geraniums, another high-value crop. Geranium cuttings infected with R3bv2 have been accidentally imported to the United States five times since 1980, triggering costly eradications. To prevent further introductions, USDA APHIS regulates offshore geranium production practices. Geraniums are typically grown from cuttings in a volcanic scoria rock medium. Reusing this growth medium saves labor and carbon. Growers must currently steam the medium at 80°C for 120 min before reuse. This required treatment is both costly and environmentally destructive. We empirically determined the conditions required to inactivate R3bv2 in infected geranium tissue with the goal of conserving resources while maintaining rigorous biosecurity. Roots of R. solanacearum-infected geraniums grown in scoria under typical production conditions were exposed to a range of time and temperatures. Surviving pathogen populations were quantified using a sensitive combination of serial dilution plating and enrichment culture. Over 99.9% of R3bv2 cells in infected roots were inactivated by exposure to 55°C dry heat for 15 min. However, these roots sometimes contained a small subpopulation of heat-resistant R3bv2 cells. The heat-resistant subpopulation was no longer detectable after infected roots were held at 75°C for 15 min. This treatment also eradicated R3bv2 cells in the stems of infected geranium plants and in infested volcanic scoria growth medium. These results demonstrate that R. solanacearum R3bv2 is eradicated from infected geranium tissue and growth media by cooler and shorter heat treatments than currently required.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-21
preprintOpen accessSenior authorAbstract Plant pathogenic Ralstonia belonging to the IIB-1 (“race 3 biovar 2”) and I-33 (rose) subgroups are emerging quarantine and biosecurity threats. Both strains have been introduced to Europe, where they persist in weedy plants and surface water and cause occasional costly disease outbreaks. We combined in planta, in vitro , and environmental water microcosm experiments to determine if these two concerning strains are likely to co-exist in environments where they have become established or if one might be expected to displace the other. Using a representative strain from each subgroup we investigated the dynamics and fitness of these two Ralstonia pathogens across ecologically relevant environments. Interactions between the strains were context dependent: the presence of a competing strain had little impact on bacterial survival in river water microcosms, but the I-33 strain had a fitness advantage in wilt susceptible tomato plants. We found no evidence of direct growth inhibition by either strain in vitro . The IIB-1 strain persisted longer than I-33 in cool temperature river water microcosms. Warmer temperatures extended the culturability of both strains, which may be important as climate change warms surface water globally. Additionally, Ralstonia strains persisting in 20°C water microcosms for 6 months were still able to cause disease in tomato plants. Together, our results provide useful insight into the dynamics of these two strains in environments where they are currently established, which may inform management practices moving forward.
Phytopathology · 2024-08-26 · 9 citations
articleSenior authorMost Ralstonia solanacearum species complex strains cause bacterial wilts in tropical or subtropical zones, but the group known as race 3 biovar 2 (R3bv2) is cool virulent and causes potato brown rot at lower temperatures. R3bv2 has invaded potato-growing regions around the world but is not established in the United States. Phylogenetically, R3bv2 corresponds to a subset of the R. solanacearum phylotype IIB clade, but little is known about the distribution of the cool virulence phenotype within phylotype IIB. Therefore, genomes of 76 potentially cool virulent phylotype IIB strains and 30 public genomes were phylogenetically analyzed. A single clonal lineage within the sequevar 1 subclade of phylotype IIB that originated in South America has caused nearly all brown rot outbreaks worldwide. To correlate genotypes with relevant phenotypes, we quantified virulence of 10 Ralstonia strains on tomato and potato at both 22 and 28°C. Cool virulence on tomato did not predict cool virulence on potato. We found that cool virulence is a quantitative trait. Strains in the sequevar 1 pandemic clonal lineage caused the most disease, whereas other R3bv2 strains were only moderately cool virulent. However, some non-R3bv2 strains were highly cool virulent and aggressively colonized potato tubers. Thus, cool virulence is not consistently correlated with strains historically classified as the R3bv2 group. To aid in the detection of sequevar 1 strains, this group was genomically delimited in the LINbase web server, and a sequevar 1 diagnostic primer pair was developed and validated. We discuss implications of these results for the R3bv2 definition.
Recent grants
Collaborative Research: Extracellular DNA: in Defense of Plant Cells
NSF · $152k · 2015–2018
Metabolic multitasking: How Ralstonia solanacearum uses nitrate for plant pathogenesis
NSF · $508k · 2013–2017
Frequent coauthors
- 41 shared
Philippe Prior
Centre de Coopération Internationale en Recherche Agronomique pour le Développement
- 26 shared
Jonathan M. Jacobs
The Ohio State University
- 25 shared
Tiffany M. Lowe‐Power
- 23 shared
Florent Ailloud
Ludwig-Maximilians-Universität München
- 13 shared
Beth L. Dalsing
University of Wisconsin–Madison
- 12 shared
Connor G. Hendrich
University of Wisconsin–Madison
- 11 shared
Taca Vancheva
Agropolis International
- 11 shared
April M. MacIntyre
University of Wisconsin–Madison
Education
- 1987
Ph.D. Plant Pathology
Virginia Polytechnic Institute and State University
- 1980
B.S. Botany
University of Maine
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