Molecular mechanisms of pattern formation in bacterial communities

Multicellularity independently evolved more than 20 times and is found in all three domains of life, suggesting an intrinsic capacity of cells to assemble into structured communities. A defining characteristic of this lifestyle is that it allows for functional diversification, ranging from physiological heterogeneity to terminal cellular differentiation. This selective advantage is reflected by the observation that bacteria are part of cellular assemblages (biofilms) under most natural settings. Yet, our thinking about the development of multicellular organisms is traditionally restricted to eukaryotes. Little attention is given to the mechanisms of structural organization in bacterial communities and how these are modulated in response to environmental changes.

bacterial colony

cross section of a tree trunk

We study cell-cell communication and biofilm development in the Gram-negative pathogen Pseudomonas aeruginosa PA14.  This bacterium produces phenazines, colorful redox-active antibiotics.  We found that P. aeruginosa can make use of phenazines as signaling molecules that regulate gene expression.  In the absence of these signals the bacteria aggregate into visually striking, wrinkled colonies, while wild type colonies are smooth.

phenazine-null mutant

wild type

Comparison of wild type and phenazine-null strains of P. aeruginosa PA14. Ten ┬Ál of cell suspensions were spotted onto 1% agar plates supplemented with Congo red.

The inset is a digital micrograph showing the wrinkled surface of the phenazine-null mutant at 200x. The wrinkles are approximately 1 mm in height.

We are interested in questions such as:

 

    Are phenazines acting as morphogens, i.e., regulating gene expression across a concentration gradient within the community?

 

    How do cells sense phenazines and transduce this information into a transcriptional response?

 

    What are the general mechanisms (such as motility or the production of extracellular matrix) that allow P. aeruginosa to aggregate into seemingly structured communities?

 

    How do environmental cues modulate the structure of these communities?