Biology subjects

Gibbs, K. A.

Publications and source records attributed to Gibbs, K. A..

8 recordsLinked to original sources

bioRxiv2026

Contact-dependent communication shapes the mesoscale spatial organization of bacterial swarms

Scientists use microscopy images to visualize and describe organisms and their interactions. Microscale visual inspections of individual cells and colonies, paired with genetic approaches, have revealed key developmental steps within microbial communities including, for example, swarms, biofilms, and fruiting bodies. However, there is a lack of formal, quantitative descriptions of these structures. This gap limits understanding of the structure and relevance of cell clusters, especially regarding development and interactions. Here, we develop biologically informed mathematical methods to formally assess cell clusters that assemble and dissolve over time in bacterial colonies. Our approaches to this analysis of the developmental stages of swarming, a type of collective migration, focus on cell length (as a proxy for developmental stage), cell-to-cell contacts, and groupings. We apply these to data from Proteus mirabilis strains with genetic disruptions in different aspects of its communication mechanisms to explore how identity signaling and cell-to-cell contact affect population structure at different scales. We found that kin recognition and contact-dependent, cell-cell communication govern population architecture during collective migration, such as swarming. This integration of microbiology with applied mathematics and computer science is a frontier for analyzing experimental data, leading to testable biological insights. SignificanceCollective behaviors are often exhibited by social organisms. Open questions regarding these behaviors include: how do communication and familial identity influence local interactions, and how do local interactions combine to create collective behaviors? Qualitative descriptions from visual examination of microbes can be useful in approaching these questions, but formal quantification of these structures will be essential if we are to understand the mechanisms that underlie organismal behavior and organization. This manuscript bridges microbiology and applied mathematics, interleaving the mathematics and the experiments in an iterative fashion. We offer critical advances to better understand, analyze, and characterize the multiscale structures that form and dissolve as a colony engages in collective migration. Our findings suggest that cell-cell communication plays an important role in population architecture, specifically that communication may "prime" cells for collective migration and prevent stagnation during life stage transitions.

microbiology↗

bioRxiv2023

Non-cognate immunity proteins provide broader defenses against interbacterial effectors in microbial communities

Dense microbial communities, like the gut and soil microbiomes, are dynamic societies. Bacteria can navigate these environments by deploying proteins that alter foreign cells behavior, such as interbacterial effectors. Current models suggest that adjacent sibling cells are protected by an immunity protein, as compared to toxin-antitoxin systems that act only within the effector-producing cell. A prevailing hypothesis is that immunity proteins binding to specific (cognate) protein partners is sufficient to disrupt effector function. Further, there is little-to-no crosstalk with other non-cognate effectors. In this research, we build on sporadic reports challenging these hypotheses. We show that immunity proteins from a newly defined protein family can bind and protect against non-cognate PD-(D/E)XK-containing effectors from diverse phyla. We describe the domains essential for binding and function and show that binding alone is insufficient for protective activity. Moreover, we found that these effector and immunity genes co-occur in individual human microbiomes. These results expand the growing repertoire of bacterial protection mechanisms and the models on how non-cognate interactions impact community structure within complex ecosystems.

microbiology↗

bioRxiv2021

The conserved serine transporter SdaC moonlights to enable self recognition

Cells can use self recognition to achieve cooperative behaviors. Self-recognition genes principally evolve in tandem with partner self-recognition alleles. However, other constraints on protein evolution could exist. Here, we have identified an interaction outside of self-recognition loci that could constrain the sequence variation of a self-recognition protein. We show that during collective swarm expansion in Proteus mirabilis, self-recognition signaling co-opts SdaC, a serine transporter. Serine uptake is crucial for bacterial survival and colonization. Single-residue variants of SdaC reveal that self recognition requires an open conformation of the protein; serine transport is dispensable. A distant ortholog from Escherichia coli is sufficient for self recognition; however, a homologous serine transporter, YhaO, is not. Thus, SdaC couples self recognition and serine transport, likely through a shared molecular interface. Understanding molecular and ecological constraints on self-recognition proteins can provide insights into the evolution of self recognition and emergent collective behaviors. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=119 SRC="FIGDIR/small/428846v1_ufig1.gif" ALT="Figure 1"> View larger version (14K): org.highwire.dtl.DTLVardef@17dbf8eorg.highwire.dtl.DTLVardef@ab0faeorg.highwire.dtl.DTLVardef@9289adorg.highwire.dtl.DTLVardef@8ccc89_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2020

A family of contact-dependent nuclease effectors contain an exchangeable, species-identifying domain

In mixed-species communities, bacteria can deploy contact-dependent effectors to compete with other organisms, often directly injecting these proteins into neighboring cells. One current hypothesis is that the entire protein contains information specific for a single species; emergence of new effectors comes from acquiring genes. Here we have characterized a family of DNA-degrading effectors that are nucleases which cause death. Like other families of chimeric nucleases, these effectors contain two domains. One is a PD-(D/E)XK-containing domain necessary for DNA cleavage. The other domain, which does not contain known DNA-binding structures, encodes species-identifying information. We capitalized on the species-identifying domain to differentiate among low-abundance species, as well as to reveal domain architectures within these proteins, in human gut and oral microbiomes. Emerging are questions about how low-abundance strains use effectors for survival and how strain-identifying effectors evolve. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=108 SRC="FIGDIR/small/956912v1_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@1be133aorg.highwire.dtl.DTLVardef@1e070d0org.highwire.dtl.DTLVardef@e8145org.highwire.dtl.DTLVardef@48dc1e_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

bioRxiv2018

Peer pressure from a Proteus mirabilis self-recognition system controls participation in cooperative swarm motility

Colonies of the opportunistic pathogen Proteus mirabilis can distinguish self from non-self: in swarming colonies of two different strains, one strain excludes the other from the expanding colony edge. Predominant models characterize bacterial kin discrimination as immediate antagonism towards non-kin cells, typically through delivery of toxin effector molecules from one cell into its neighbor. Upon effector delivery, receiving cells must either neutralize it by presenting a cognate anti-toxin, as would a clonal sibling, or suffer cell death or irreversible growth inhibition, as would a non-kin cell. Here we expand this paradigm to explain the non-lethal Ids self-recognition system, which stops access to a cooperative social behavior in P. mirabilis through a distinct mechanism: selectively and transiently inducing nonself cells into a lifestyle incompatible with cooperative swarming. This state is characterized by reduced expression of genes associated with protein synthesis, virulence, and motility, and also causes non-self cells to tolerate previously lethal concentrations of antibiotics. We found that entry into this state requires a temporary activation of the stringent response in non-self cells and results in the iterative exclusion of non-self cells as a swarm colony migrates outwards. These data clarify the intricate connection between non-lethal recognition and the lifecycle of P. mirabilis swarm colonies.

microbiology↗

bioRxiv2018

Swarming bacteria respond to increasing barriers to motility by increasing cell length and modifying colony structure

Organisms can alter morphology and behaviors in response to environmental stimuli such as mechanical forces exerted by surface conditions. The bacterium Proteus mirabilis responds to surface-based growth by enhancing cell length and degree of cell-cell interactions. Cells grow as approximately 2-micrometer rigid rods and independently swim in liquid. By contrast on hard agar surfaces, cells elongate up to 40-fold into snake-like cells that move as a collective group across the surface. Here we have elucidated that individual cell size and degree of cell-cell interactions increased across a continuous gradient that correlates with increasing agar density. We further demonstrate that interactions between the lipopolysaccharide (LPS) component of the outer membrane and the immediate local environment modified these responses by reducing agar-associated barriers to motility. Loss of LPS structures corresponded with increased cell elongation on any given surface. These micrometer-scale changes to cell shape and collective interactions corresponded with centimeter-scale changes in the overall visible structure of the swarm colony. It is well-appreciated in eukaryotes that mechanical forces impact cell shape and migration. Here we propose that bacteria can also dynamically respond to the mechanical forces of surface conditions by altering cell shape, individual motility, and collective migration.

microbiology↗

bioRxiv2017

A proposed chaperone of the bacterial type VI secretion system functions to constrain a self-identity protein

The opportunistic bacterial uropathogen Proteus mirabilis can communicate identity through the export of the self-identity protein, IdsD, via the type VI secretion (T6S) system. Expression of the ids genes provides a fitness advantage during polymicrobial infections in a mouse infection model. Here we provide an answer to the unresolved question of how the activity of a T6S substrate, such as IdsD, is regulated before export. We demonstrate that IdsD is found in clusters that form independently of the T6S machinery and activity. We show that the protein IdsC, which is a member of the proposed DUF4123 chaperone family, is essential for the stability of these clusters as well as the IdsD protein itself. And we provide evidence that amino acid disruptions in IdsC are sufficient to disrupt IdsD export but not IdsD localization into stable subcellular clusters, strongly supporting that IdsC functions in at least two different ways: IdsD stabilization and IdsD export. We propose that IdsC, and likely other DUF4123-containing proteins, function to regulate T6S substrates before export by both stabilizing the protein and mediating export at the T6S machinery.

microbiology↗

bioRxiv2017

A single point mutation in a TssB/VipA homolog disrupts sheath formation in the type VI secretion system of Proteus mirabilis

The type VI secretion (T6S) system is a molecular device for the delivery of proteins from one cell into another. T6S function depends on the contractile sheath comprised of TssB/VipA and TssC/VipB proteins. We previously reported on a mutant variant of TssB that disrupts T6S-dependent export of the self-identity protein, IdsD, in the bacterium Proteus mirabilis. Here we determined the mechanism underlying that initial observation. We show that T6S-dependent export of multiple self-recognition proteins is abrogated in this mutant strain. We have mapped the mutation, which is a single amino acid change, to a region predicted to be involved in the formation of the TssB-TssC sheath. We have demonstrated that this mutation does indeed inhibit sheath formation, thereby explaining the global disruption of T6S activity. We propose that this mutation could be utilized as an important tool for studying functions and behaviors associated with T6S systems.

microbiology↗