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DSSS: Why Changing Color Matters to Pseudomonas Aeruginosa2 min read

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Dianne Newman's research focuses on understanding the coevolution of microbial metabolism and environmental chemistry. The contexts that motivate her research span ancient sedimentary deposits to chronic infections. Her work is helping to reshape interpretations of ancient molecular fossils as well as redox-active "secondary" metabolites.  Dianne earned her PhD in Environmental Engineering at MIT with Francois Morel, a geochemist, and trained as a postdoc at Harvard Medical School with Roberto Kolter, a bacterial geneticist.  She is a Professor of Biology and Geobiology at Caltech, and an Investigator of the Howard Hughes Medical Institute.

Abstract

One of the defining attributes of Pseudomonas aeruginosa is its striking blue-green color.  The name “aeruginosa” derives from the Latin word for copper rust, which is of the same hue.  While microbiologists and clinicians have long used color to identify the organism, why it is colored in the first place—and why its color changes with aeration—is a question that not many have considered.  We now know that phenazines, a class of redox-active pigments, are responsible not only for the blue-green color of P. aeruginosa in the presence of oxygen, but also for different colors displayed by other Pseudomonas species.  In the early 20th century, Ernst Friedheim and colleagues postulated that phenazines are “accessory respiratory pigments” that sustain bacterial “respiration” based on their ability to stimulate oxygen consumption.  Their work was carried out before respiratory pathways were fully understood and well before the importance of microbial biofilms in nature and disease was widely recognized.  In the interval between Friedheim’s pioneering studies and our recent work, attention shifted to exploring the roles of phenazines as virulence factors.  Phenazines came to be known as "secondary metabolites", molecules produced at late stages of microbial growth in laboratory cultures whose function was thought to be to protect Pseudomonas species from competitors.  While the antibiotic activity of phenazines has been elegantly shown in a variety of contexts, labeling phenazines as “secondary metabolites” suggests that they are not essential to the growth or survival of their producers.  In this talk, I will present a body of work that champions Friedheim’s original hypothesis and goes beyond it.  Specifically, I will discuss a variety of important physiological functions phenazines play for P. aeruginosa under anoxic conditions that transcend their antibiotic activity, including controlling carbon flux through central metabolic pathways, redox homeostasis, iron acquisition, survival in multicellular communities, and cell-cell signaling.  I will close by discussing the implications of these findings for treating cystic fibrosis infections.