David Guttman, PhD

Professor
Department(s): Cell & Systems Biology, Ecology & Evolutionary Biology
Location: Earth Sciences Centre, 25 Willcocks St.
Email: david.guttman@utoronto.ca

The Guttman lab aims to understand how bacteria adapt to, and manipulate their hosts. The lab integrates evolutionary and comparative genomics, molecular and functional biology, and computational & statistical analyses to identify bacterial virulence factors and characterize their role in host specificity and host immune modulation. His group focuses on a number of related questions, including: the evolution and function of secreted effectors, which can either promote bacterial virulence or elicit host immunity depending on the specific host-microbe interaction; very fine-scale evolutionary genomic studies of host-associated bacterial populations to determine how lineages evolve over the course of disease development; and the characterization of microbial community (microbiome) diversity in plant and human hosts.

Selected publications:

  1. Sheppard SK, Guttman DS, Fitzgerald JR. (2018) Population genomics of bacterial host adaptation. Nature Review Genetics. doi: 10.1038/s41576-018-0032-z
  2. Layeghifard M, Hwang DM, Guttman DS (2017) Disentangling interactions in the microbiome: A network perspective. Trends in Microbiology. 25(3):217-228.
  3. Mott GA, Thakur S, Smakowska E, Wang PW, Belkhadir Y, Desveaux D, Guttman DS (2016) Genomic screens identify a new phytobacterial microbe-associated molecular pattern and the cognate Arabidopsis receptor-like kinase that mediates its immune elicitation. Genome Biology 17(1):98.
  4. Diaz Caballero J, ST Clark, B Coburn, Y Zhang, PW Wang, S Donaldson, DE Tullis, YCW Yau, VJ Waters, DM Hwang, DS Guttman (2015) Selective sweeps and parallel pathoadaptation drive Pseudomonas aeruginosa evolution in the cystic fibrosis lung. mBio 6(4):e00981-15.
  5. Lewis JD, Lee AH, Hassan JA, Wan J, Hurley B, Jhingree JR, Wang PW, Lo T, Youn JY, Guttman DS†, Desveaux D† (2013) The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a. Proceedings of the National Academy of Sciences, USA, 110(46): 18722-18727.
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