Unsere Forschung fokussiert darauf generelle ökologische Prinzipien, die sich mit den Ursachen und Konsequenzen von mikrobieller Diversität befassen, abzuleiten und zu testen. Wir wollen die folgenden zwei zentralen Fragen der mikrobiellen Ökologie beantworten:
Wieso gibt es in mikrobiellen Gemeinschaften so viele verschiedene Zelltypen? In anderen Worten: was verhindert, dass ein paar wenige Zelltypen evolvieren, die sich durchsetzen und die anderen verdrängen?
Ist Diversität ein wichtiger Faktor der funktionalen Leistung von mikrobiellen Gemeinschaften? Falls ja, was sind die Mechanismen, die dafür verantwortlich sind?
Wir verwenden eine Kombination aus Laborexperimenten und der Untersuchung von Umweltsystemen um diese Fragen zu beantworten. Die Ursachen von mikrobieller Diversität untersuchen wir mittels experimenteller Systeme und fokussieren dabei insbesondere auf das Konzept der metabolischen Spezialisierung. Die zentrale Hypothese ist hierbei, dass gewisse metabolische Prozesse miteinander inkompatibel sind und deshalb am effizientesten in verschiedenen Zelltypen ausgeführt werden. Dies führt letztlich dazu, dass Diversität entsteht. Um diese Hypothese zu testen, messen wir in Laborexperimenten die Effekte von Interaktionen zwischen verschiedenen metabolischen Prozessen und verfolgen ihr Schicksal über evolutionäre Zeiträume.
Um die Konsequenzen mikrobieller Diversität zu untersuchen, untersuchen wir Umweltsysteme. Die zentrale Hypothese ist hierbei, dass mikrobielle Diversität ein wichtiger Faktor für die funktionale Leistung von Ökosystemen ist. Um dies zu testen, messen wir die Raten und das Ausmass von verschiedenen metabolischen Prozessen in Umweltsystemen und untersuchen ob es einen Zusammenhang mit dem Ausmass der Diversität in diesen Systemen gibt. Wir manipulieren dann experimentell das Ausmass der Diversität und werten die Konsequenzen für die verschiedenen metabolischen Prozesse aus. Das Ziel ist letztlich unser Verständnis darüber zu verbessern was Diversität in der Umwelt begünstigt und wieso Diversität ein wichtiger Faktor für die funktionale Leistung von Ökosystemen sein könnte.
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authors => protected'Han, M.; Ruan, C.; Wang, G.; Johnson, D. R.' (68 chars)
title => protected'Evaporation controls contact-dependent bacterial killing during surface-asso ciated growth' (89 chars)
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categories => protected'bacterial interactions; contact-dependent killing; antagonism; T6SS; evapora tion; vibrio cholerae' (97 chars)
description => protected'Many bacteria employ contact-dependent killing mechanisms, which require dir ect physical contact with a target cell, to gain an advantage over competito rs. Here, we hypothesize that evaporation-induced fluid flows determine the number of contacts between attacking and target cells, thus controlling kill ing efficacy. To test this, we experimentally manipulated the strength of th e coffee ring effect (CRE) and measured the consequences on killing mediated by the type VI secretion system (T6SS). The CRE is caused by evaporation-in duced fluid flows that move water and cells from the center to the periphery of a liquid droplet, consequently concentrating cells at the periphery. We found that the CRE significantly increases the number of contacts between at tacking (<em>Vibrio cholerae</em>) and target (<em>Escherichia coli</em>) ce lls and enhances the ability of<em> V. cholerae</em> to kill and out-compete <em>E. coli</em>. We corroborated our findings with individual-based comput ational simulations and demonstrated that increased cell densities at the dr oplet periphery caused by the CRE increase killing. We further found that th e T6SS firing rate, lethal hit threshold, and lysis delay significantly affe ct killing when the CRE is strong. Our results underscore the importance of evaporation-induced fluid flows in shaping bacterial interactions and contro lling competitive outcomes.' (1395 chars)
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authors => protected'Ruan, C.; Ramoneda, J.; Kan, A.; Rudge, T. J.; Wang , G.; Johnson, D. R.' (111 chars)
title => protected'Phage predation accelerates the spread of plasmid-encoded antibiotic resista nce' (79 chars)
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description => protected'Phage predation is generally assumed to reduce microbial proliferation while not contributing to the spread of antibiotic resistance. However, this assu mption does not consider the effect of phage predation on the spatial organi zation of different microbial populations. Here, we show that phage predatio n can increase the spread of plasmid-encoded antibiotic resistance during su rface-associated microbial growth by reshaping spatial organization. Using t wo strains of the bacterium <em>Escherichia coli</em>, we demonstrate that p hage predation slows the spatial segregation of the strains during growth. T his increases the number of cell-cell contacts and the extent of conjugation -mediated plasmid transfer between them. The underlying mechanism is that ph age predation shifts the location of fastest growth from the biomass periphe ry to the interior where cells are densely packed and aligned closer to para llel with each other. This creates straighter interfaces between the strains that are less likely to merge together during growth, consequently slowing the spatial segregation of the strains and enhancing plasmid transfer betwee n them. Our results have implications for the design and application of phag e therapy and reveal a mechanism for how microbial functions that are delete rious to human and environmental health can proliferate in the absence of po sitive selection.' (1385 chars)
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title => protected'Metabolic interactions control the transfer and spread of plasmid-encoded an tibiotic resistance during surface-associated microbial growth' (138 chars)
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description => protected'Surface-associated microbial systems are hotspots for the spread of plasmid- encoded antibiotic resistance, but how surface association affects plasmid t ransfer and proliferation remains unclear. Surface association enables prolo nged spatial proximities between different populations, which promotes plasm id transfer between them. However, surface association also fosters strong m etabolic interactions between different populations, which can direct their spatial self-organization with consequences for plasmid transfer and prolife ration. Here, we hypothesize that metabolic interactions direct the spatial self-organization of different populations and, in turn, regulate the spread of plasmid-encoded antibiotic resistance. We show that resource competition causes populations to spatially segregate, which represses plasmid transfer . In contrast, resource cross-feeding causes populations to spatially interm ix, which promotes plasmid transfer. We further show that the spatial positi onings that emerge from metabolic interactions determine the proliferation o f plasmid recipients. Our results demonstrate that metabolic interactions ar e important regulators of both the transfer and proliferation of plasmid-enc oded antibiotic resistance.' (1243 chars)
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authors => protected'Ma, Y.; Ramoneda, J.; Johnson, D. R.' (56 chars)
title => protected'Timing of antibiotic administration determines the spread of plasmid-encoded antibiotic resistance during microbial range expansion' (131 chars)
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description => protected'Plasmids are the main vector by which antibiotic resistance is transferred b etween bacterial cells within surface-associated communities. In this study, we ask whether there is an optimal time to administer antibiotics to minimi ze plasmid spread in new bacterial genotypes during community expansion acro ss surfaces. We address this question using consortia of <em>Pseudomonas stu tzeri</em> strains, where one is an antibiotic resistance-encoding plasmid d onor and the other a potential recipient. We allowed the strains to co-expan d across a surface and administered antibiotics at different times. We find that plasmid transfer and transconjugant proliferation have unimodal relatio nships with the timing of antibiotic administration, where they reach maxima at intermediate times. These unimodal relationships result from the interpl ay between the probabilities of plasmid transfer and loss. Our study provide s mechanistic insights into the transfer and proliferation of antibiotic res istance-encoding plasmids within microbial communities and identifies the ti ming of antibiotic administration as an important determinant.' (1126 chars)
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Evaporation controls contact-dependent bacterial killing during surface-associated growth
Many bacteria employ contact-dependent killing mechanisms, which require direct physical contact with a target cell, to gain an advantage over competitors. Here, we hypothesize that evaporation-induced fluid flows determine the number of contacts between attacking and target cells, thus controlling killing efficacy. To test this, we experimentally manipulated the strength of the coffee ring effect (CRE) and measured the consequences on killing mediated by the type VI secretion system (T6SS). The CRE is caused by evaporation-induced fluid flows that move water and cells from the center to the periphery of a liquid droplet, consequently concentrating cells at the periphery. We found that the CRE significantly increases the number of contacts between attacking (Vibrio cholerae) and target (Escherichia coli) cells and enhances the ability of V. cholerae to kill and out-compete E. coli. We corroborated our findings with individual-based computational simulations and demonstrated that increased cell densities at the droplet periphery caused by the CRE increase killing. We further found that the T6SS firing rate, lethal hit threshold, and lysis delay significantly affect killing when the CRE is strong. Our results underscore the importance of evaporation-induced fluid flows in shaping bacterial interactions and controlling competitive outcomes.
Han, M.; Ruan, C.; Wang, G.; Johnson, D. R. (2025) Evaporation controls contact-dependent bacterial killing during surface-associated growth, ISME Communications, 5(1), ycaf034 (5 pp.), doi:10.1093/ismeco/ycaf034, Institutional Repository
Phage predation accelerates the spread of plasmid-encoded antibiotic resistance
Phage predation is generally assumed to reduce microbial proliferation while not contributing to the spread of antibiotic resistance. However, this assumption does not consider the effect of phage predation on the spatial organization of different microbial populations. Here, we show that phage predation can increase the spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth by reshaping spatial organization. Using two strains of the bacterium Escherichia coli, we demonstrate that phage predation slows the spatial segregation of the strains during growth. This increases the number of cell-cell contacts and the extent of conjugation-mediated plasmid transfer between them. The underlying mechanism is that phage predation shifts the location of fastest growth from the biomass periphery to the interior where cells are densely packed and aligned closer to parallel with each other. This creates straighter interfaces between the strains that are less likely to merge together during growth, consequently slowing the spatial segregation of the strains and enhancing plasmid transfer between them. Our results have implications for the design and application of phage therapy and reveal a mechanism for how microbial functions that are deleterious to human and environmental health can proliferate in the absence of positive selection.
Ruan, C.; Ramoneda, J.; Kan, A.; Rudge, T. J.; Wang, G.; Johnson, D. R. (2024) Phage predation accelerates the spread of plasmid-encoded antibiotic resistance, Nature Communications, 15, 5397 (12 pp.), doi:10.1038/s41467-024-49840-7, Institutional Repository
Metabolic interactions control the transfer and spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth
Surface-associated microbial systems are hotspots for the spread of plasmid-encoded antibiotic resistance, but how surface association affects plasmid transfer and proliferation remains unclear. Surface association enables prolonged spatial proximities between different populations, which promotes plasmid transfer between them. However, surface association also fosters strong metabolic interactions between different populations, which can direct their spatial self-organization with consequences for plasmid transfer and proliferation. Here, we hypothesize that metabolic interactions direct the spatial self-organization of different populations and, in turn, regulate the spread of plasmid-encoded antibiotic resistance. We show that resource competition causes populations to spatially segregate, which represses plasmid transfer. In contrast, resource cross-feeding causes populations to spatially intermix, which promotes plasmid transfer. We further show that the spatial positionings that emerge from metabolic interactions determine the proliferation of plasmid recipients. Our results demonstrate that metabolic interactions are important regulators of both the transfer and proliferation of plasmid-encoded antibiotic resistance.
Ma, Y.; Kan, A.; Johnson, D. R. (2024) Metabolic interactions control the transfer and spread of plasmid-encoded antibiotic resistance during surface-associated microbial growth, Cell Reports, 43(9), 114653 (17 pp.), doi:10.1016/j.celrep.2024.114653, Institutional Repository
Timing of antibiotic administration determines the spread of plasmid-encoded antibiotic resistance during microbial range expansion
Plasmids are the main vector by which antibiotic resistance is transferred between bacterial cells within surface-associated communities. In this study, we ask whether there is an optimal time to administer antibiotics to minimize plasmid spread in new bacterial genotypes during community expansion across surfaces. We address this question using consortia of Pseudomonas stutzeri strains, where one is an antibiotic resistance-encoding plasmid donor and the other a potential recipient. We allowed the strains to co-expand across a surface and administered antibiotics at different times. We find that plasmid transfer and transconjugant proliferation have unimodal relationships with the timing of antibiotic administration, where they reach maxima at intermediate times. These unimodal relationships result from the interplay between the probabilities of plasmid transfer and loss. Our study provides mechanistic insights into the transfer and proliferation of antibiotic resistance-encoding plasmids within microbial communities and identifies the timing of antibiotic administration as an important determinant.
Ma, Y.; Ramoneda, J.; Johnson, D. R. (2023) Timing of antibiotic administration determines the spread of plasmid-encoded antibiotic resistance during microbial range expansion, Nature Communications, 14(1), 3530 (12 pp.), doi:10.1038/s41467-023-39354-z, Institutional Repository
Projekte
Die plasmid-vermittelte Ausbreitung von Antibiotikaresistenzen (AR) innerhalb von und zwischen mikrobiellen Gemeinschaften ist eines der drängendsten Probleme unserer Gesellschaft, doch sind die Ursachen und potenziellen Abhilfemaßnahmen nach wie vor unklar.
