Department of Plant Pathology & Envrionmental Microbiology, Pennsylvania State
Dr. Kevin Hockett will join Penn State’s Department of Plant Pathology and Environmental Microbiology (PPEM) on February 1, 2017. Hockett is currently a USDA NIFA Postdoctoral Fellow at the University of Arizona. His research program focuses on the genetics and ecology of specialized "antibotics," called bacteriocins, used by plant-associated bacteria to compete against each other, evolutionary history of these microbe-microbe and plant-microbe interactions, and ways of using these bacteria-produced antibotics to develop new methods to control plant pathogens. He uses an integrative approach, combining bacterial genetics, genomics, transcriptomics, phylogenetics, and molecular biology in his research.
A native Oregonian, Hockett received his bachelor’s degree in microbiology from Oregon State University, and a doctorate in microbiology from the University of California, Berkeley. He has a strong commitment to teaching and mentoring. At Berkeley, he was an instructor in a synthetic course on the application of molecular technology for solving environmental problems. He further honed his pedagogical skills by teaching as an adjunct instructor at Pima Community College, a Hispanic Serving Institution in Tucson, Arizona, in addition to mentoring numerous students in laboratory-based microbiology.
Hockett will join PPEM as an Assistant Professor of Microbial Ecology and will be a Lloyd Huck Early Career Professor in the Huck Institute of Life Sciences. He fills the first position offered in the university-wide Microbiome Initiative cluster hire initiated by the College of Agricultural Sciences and the Huck.
Abstract: Plant-associated bacteria live in complex microbial communities, where they compete for limited nutrients. Plant inhabitants, including Pseudomonas syringae, commonly encode bacteriocins, proteinaceous toxins that inhibit the growth of related bacteria. As a start to understand the potential role of bacteriocins in structuring plant microbial communities, we screened 18 P. syringae isolates representing a significant portion of the phylogenetic diversity of this species. Despite the numerous computationally predicted bacteriocin loci, we found that the dominant killing was actually derived from an unpredicted bacteriophage tail-derived bacteriocin (termed tailocin). This tailocin is evolutionarily distinct from the well described tailocins of Pseudomonas aeruginosa, despite being encoded within a conserved genomic region. Multiple lines of evidence indicate lipopolysaccharide (LPS) serves as the tailocin cell surface receptor. We recovered several spontaneous tailocin-resistant mutants within two different pathovars (pv. glycinea and pv. phaseolicola). Following infiltration into their host plants (soy and green bean, respectively), nearly all mutants exhibited a plant growth defect over 48 hours of growth, compared to their wild type counterparts. In addition to recovering spontaneous tailocin-resistant mutants, we screened a collection of P. syringae mutants with insertions disrupting core LPS biosynthesis genes. In addition to these strains exhibiting tailocin-resistance (an expected result), they had gained de novo sensitivity to a non-tailocin bacteriocin produced by the same organism, which was a completely unexpected result. To our knowledge, this is the first example of such a trade-off of sensitivity, or conditionally redundant targeting, between two distinct bacteriocins produced by the same strain. Future research efforts aim to identify the receptor for the non-tailocin bacteriocin, as well as understand the underlying cause of the trade-off between sensitivities. In total, this research suggests the importance of bacteriocins in the ecology and evolution of P. syringae and potentially other plant-associated bacteria.
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