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             Karin Sauer, PhD in Microbiology and Biochemistry

             Co-Director, Binghamton Center for Biofilm Research

             Professor, Department of Biological Sciences

            Office: BI-2401


            Phone: 607-777-3157



Short Bio: Karin Sauer obtained her undergraduate degree in biology and her Diplome in Microbiology from the Philipps University in Marburg, Germany. She received her PhD in Microbiology from the Max-Planck Institute for Terrestrial Microbiology in 1999, under the guidance of Professor R.K. Thauer,and was awarded the Otto Hahn Medal and the VAAM dissertation award in 2000 for her research focusing on methanol activation and methyl group transfer by the methyltransferase isolated from Methanosarcina barkeri. Her postdoctoral work with Anne Camper at the Center for Biofilm Engineering at Montana State University in Bozeman, and her subsequent research at Binghamton University, led to the discovery that surface attachment by Pseudomonas sp. not only coincides with significant changes at the transcript and protein levels and but that subsequent formation of biofilms occurs in a progressive and stage-specific manner with each stage displaying a distinct phenotype. Sauer joined the faculty in the Department of Biological Sciences at Binghamton University in 2002. She is now a professor there and the co-director of the newly established Binghamton Biofilm Research Center (BBRC). 

Research interests: My research group utilizes the model organism Pseudomonas aeruginosa to elucidating regulatory and signaling events underlying the formation and development of highly antimicrobial resistant biofilms. Specifically, we are interested differential gene expression coinciding with the formation and dispersion of biofilms, the role of posttranslational modifications in enabling bacteria to sense and respond to environmental conditions, and the mechanism by which biofilm cells gain their heightened resistance to antimicrobial agents. The overall goal of our research to identify factors to control and manage biofilms and their extraordinary resistance to antimicrobial agents.

Biofilm focus: My research on biofilms focuses on biofilm development, biofilm dispersion, and biofilm tolerance. For instance, bacterial cells within biofilms exhibit elevated levels of tolerance towards antimicrobial agents, rendering biofilm infections difficult to eradicate via conventional treatment regimens. In Pseudomonas aeruginosa, biofilm tolerance is linked to biofilm development, with transition to the irreversible attachment stage, regulated by the two-component sensorhybrid SagS, marking the timing when biofilms switch to the high-level tolerance phenotype. Recent findings furthermore suggest in this developmental process, the two-component sensor SagS plays a dual role (i) by promoting the switch from the planktonic to the biofilm mode of growth and (ii) by enabling biofilm cells to gain their heightened tolerance by indirectly activating BrlR, a transcriptional regulator of biofilm resistance. Ongoing research focuses on elucidating the mechanism by which the membrane-bound protein SagS carries out both functions. Dispersion of P. aeruginosa biofilms occurs in response to a wide array of environmental cues including carbon sources and nitric. Dispersion in response to carbon sources requires the sensory protein NicD while dispersion in response to NO requires the membrane bound protein NbdA. Independent of the dispersion cue, dispersion furthermore requires the chemotactic protein BdlA, diguanylate cyclase GcbA, and phosphodiesterases (PDEs, e.g. DipA, RbdA), and coincides with increased PDE activity and a reduction of c-di-GMP levels. It is now apparent that these proteins form a membrane associated complex and are part of a signal transduction pathway required to sense dispersion cues and, via a series of posttranslational modifications, translate dispersion cue perception across cellular compartments into the modulation of the intracellular c-di-GMP pool. However, subsequent events leading to bacterial cells dispersing from the biofilm and XXX are unknown. Ongoing research aims at elucidating genes necessary to enable dispersion. Considering the similarity of the dispersion response regardless of the dispersion-inducing conditions used, we hypothesized that, while dispersion events can be initiated by a variety of cues, subsequent events enabling dispersion and the phenotypic switch require differential expression of a common set of genes.

Techniques: We use a variety of techniques to tackle our research projects. These include bacteriology, biochemistry (Western blot, pulldown assays, protein purification, enzyme assays, detection and quantitation of small molecules), proteomics (2D/PAGE, protein identification by mass spectrometry), molecular biology (qPCR, cloning, tagging, gene inactivation, site-directed mutagenesis, reporter genes, site-directed mutagenesis, EMSAs) and genomic approaches (RNA-Seq, ChIP-Seq, using next-generation sequencing). Additionally, my lab has extensive expertise in growing, analyzing and quantitating biofilms grown under static and flowing conditions by microscopy, spectroscopic and fluorescence-based methods including FACS and viability counts.

Last Updated: 6/14/17