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Indiana University Bloomington

Department of Biology

Faculty & Research

Faculty Profile

Daniel Kearns

Photo of Daniel Kearns
Research Images
Research photo by Daniel Kearns

Plate series of swarming behaviors.

Research photo by Daniel Kearns

Motility is inhibited in cell aggregates (membranes stained in red) by puncta of the EpsE clutch protein (colored green).

Research photo by Daniel Kearns

Population heterogeneity and bistable gene expression. Left: phase contrast. Right : epifluorescence. Exponential phase cultures grow as a heterogeneous mixture of short, motile cells and non-motile chains. All cells contain the motility gene transcriptional reporter construct (Pflagellin-GFP) but only the short, motile cells express GFP (false colored in green). The membranes of all cells were stained and false colored in red.

Research photo by Daniel Kearns

Cross-section diagrams of the B. subtilis flagellar basal body. “Planktonic” cells are motile because FliG interacts with MotA to transduce the power of proton flow into the power of flagellar rotation. In “biofilm” cells, EpsE disables flagellar rotation by disrupting the FliG-MotA interaction. Dark grey rectangles indicate the plasma membrane. Light grey rectangles indicate the peptidoglycan cell wall. "G" indicates the rotor FliG. "M" indicates the switch protein, FliM. "E" indicates EpsE. Hexagons indicate the biofilm "EPS" matrix.

Professor of Biology

IU Affiliations
Center for the Integrative Study of Animal Behavior

Contact Information
By telephone: 812-856-2523/6-2559(lab)
JH 469/JH 432 (lab)
Research Areas
  • Microbial Cell Biology and Environmental Responses
  • Microbial Interactions and Pathogenesis

Ph.D., University of Georgia, 2000
Postdoctoral Fellow, Harvard University, 2000-2004

Research Description

Multicellular behavior and bacterial domestication. Bacteria were long thought to take up nutrients, grow, and divide as individual unicellular organisms. However, this strict unicellular view has been challenged by the discovery of bacterial cell-to-cell communication systems and the observation of rudimentary multicellular behaviors. Perhaps one reason that bacterial multicellularity had gone unnoticed was the fact our cultivation techniques have selected against cell-cell interactions in favor of rapid growth as dispersed cells. Such is the case for our model system of choice, Bacillus subtilis. Laboratory strains of B. subtilis have been selected for ease of manipulation to create a powerful model genetic system at the expense of more complex biology. Our research returns to the study of wild strains of B. subtilis and two of the multicellular behaviors that were lost during laboratory strain domestication: swarming motility and biofilm formation. Each behavior appears to be an opposing and exclusive multicellular state in which swarming favors population dispersal while biofilm formation favors persistence.

Swarming motility. Swarming motility is a social form of migration in which cells associate in multicellular clusters to cooperatively propel a population over solid surfaces. Swarming is similar to swimming motility in that both motile behaviors are powered by rotating flagella. However, unlike swimming, swarming requires a solid surface, surfactant secretion, and a critical cell density. We have identified a variety of mutations that specifically impair swarming motility and many of these mutations are within genes of previously unknown function. Our lab uses a combination classical genetics, molecular genetics, and biochemistry to dissect the function of these unusual swarming specific genes.

Bistability and motility development. Through the study of swarming motility genes we discovered that B. subtilis grows a heterogeneous mixed population of short motile cells and long non-motile chains. This heterogeneity is a form of development that is governed by a bistable regulatory switch that turns motility gene expression ON in motile cells and OFF in chains. Proteins required for swarming motility, SwrA and SwrB, bias the switch in favor of the motile ON state. SwrA is of particular interest as the swrA gene is mutated in laboratory strains and contributes to the inability of domesticated strains to swarm. Future work will focus on investigating the molecular mechanisms of SwrA, SwrB, and the bistable switch that controls motility. In addition, we would like to explore the distribution of swarming motility genes in other wild isolates to assess the prevalence of swarming in the environment. By determining the presence and functionality of such genes in different natural isolates, we hope to gain insight into the evolutionary benefits and ecological roles of swarming motility.

Transition from motility to biofilm formation.  B. subtilis creates architecturally complex, sessile aggregates called biofilms and like swarming motility, biofilm formation is robust in undomesticated strains but severely attenuated in laboratory strains. Of critical importance to biofilm architecture is the master transcriptional regulator SinR. SinR mediates the transition from motility to biofilm formation by directly repressing the 15 gene eps operon required for the synthesis of a biofilm-stabilizing extracellular polysaccharide matrix. Also encoded within the eps operon is a protein, EpsE, that acts like a clutch on the flagellar motor. Thus the transition from motility to biofilm formation is determined at a single locus: when biofilm formation is initiated, SinR derepresses the eps operon, the matrix EPS is synthesized, and flagellar rotation is simultaneously inhibited.

Clutch control. Flagella are composed of nearly 40 proteins that cooperate to assemble a long helical filament. The cells rotate the filament like a propeller to push themselves through the environment. At the base of the flagellum is a series of proton channels (made of MotA and MotB) that interact with a wheel-like rotor (made of FliG). As protons flow through the channels, conformational changes in MotA cause FliG to turn and cause rotation of the flagellum. The motility inhibitor protein EpsE interacts with FliG to disrupt interaction with MotA, and like a clutch, disconnects the drive train from the power source to arrest flagellar rotation. We study the mechanistic basis of the EpsE clutch protein and the consequence of clutch activity on biofilm formation. Biofilm formation of pathogens is often an important stage in virulence and if we can trick pathogenic bacteria into remaining motile by targeting clutching mechanisms, their biofilms might be destabilized.

Goal. The overall goal of the lab is to identify, characterize, and understand new genetic components of multicellular behavior in undomesticated B. subtilis. With this information, we hope to create a larger model that explains how swarming motility and biofilm formation interact and in which environments each is favored.

Select Publications
Winkelman, JT, Blair, KM, and DB Kearns.  2009.  RemA (YlzA) and RemB (YaaB) regulate extracellular matrix operon expression and biofilm formation in Bacillus subtilis.  J. Bacteriol. 191, 3981-3991.
Chen R, Guttenplan, SB, Blair, KM, and DB Kearns.  2009.  Role of the σD-dependent autolysins in Bacillus subtilis population heterogeneity.  J. Bacteriol. 191, 5775-5784.
Patrick, JE, and DB Kearns. 2008. MinJ (YvjD) is a topological determinant of cell division in Bacillus subtilis. Mol Microbiol 70:1166-1179.
Blair, KM, L Turner, J Winkelman, HC Berg, and DB Kearns. 2008. A molecular clutch disables flagella in the Bacillus subtilis biofilm. Science 320: 1636-1638.
Chu, F, DB Kearns, SS Branda, R Kolter, and R Losick.  2006.  Targets of the master regulator of biofilm formation in Bacillus subtilisMol Microbiol 59:1216-1228.
Kearns, DB, F Chu, SS Branda, R Kolter, and R Losick.  2005.  A master regulator for biofilm formation by Bacillus subtilisMol Microbiol  55: 739-749.
Kearns, DB, and R Losick.  2005.  Cell population heterogeneity during growth of Bacillus subtilisGenes Dev 19:3083-3094. 
Kearns, DB, F Chu, R Rudner, and R Losick.  2004.  Genes governing swarming motility in Bacillus subtilis and evidence for a phase variation mechanism controlling surface motility.  Mol Microbiol  52: 357-369.
Kearns, DB, and R Losick.  2003.  Swarming motility in undomesticated Bacillus subtilisMol Microbiol  49: 581-590.

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