Jyl S. Matson, Ph.D.
Associate Professor
Vibrio cholerae stress response mechanisms and pathogenesis
Office: HEB 243
Telephone: 419-383-3971
Fax:听 419-383-3002
E-mail: jyl.matson@utoledo.edu
Cholera, an epidemic disease characterized by voluminous watery diarrhea, is produced when the Gram negative curved bacillus Vibrio cholerae colonizes the upper small intestine of its human host. V. cholerae are found throughout the world in coastal areas and are transmitted to humans through consumption of contaminated food or water. Despite its long history as a research target, cholera continues to afflict approximately 5 million people each year and remains an important public health problem in many areas of the globe.
Antibiotics are important adjuncts to oral rehydration therapy in cholera disease management. However, due to the rapid emergence of resistance to the antibiotics used to treat cholera, therapeutic options are becoming limited. There is, therefore, a critical need to develop additional therapeutics to aid in the treatment of cholera. One of the goals of the Matson lab is to identify and characterize small molecule inhibitors of the extracytoplasmic stress response (sE) pathway of V. cholerae. This pathway is required for virulence of V. cholerae and overall fitness of the bacteria in the presence of extracellular stress. Compounds identified using high throughput screening will have the potential to be developed into therapeutic agents against cholera. These compounds will also be valuable probes for uncovering basic molecular mechanisms of an important cause of diarrheal disease.
Another aspect of Dr. Matson鈥檚 research is using next generation sequencing (RNAseq) to uncover new knowledge about how bacteria respond to various stressors. 听Our lab is particularly interested in using RNAseq to determine the function of previously uncharacterized V. cholerae proteins. 听We have performed RNAseq analysis on V. cholerae grown in the presence and absence of sublethal concentrations of antimicrobial peptides to determine the overall transcriptional response of the bacteria to this type of stress. We are currently following up on a tremendous amount of data to determine the importance of differentially expressed genes in these conditions. 听
听Dr. Matson received her Ph.D. in Microbiology and Immunology from the University of North Dakota under the mentorship of Dr. Matthew Nilles. She then completed her postdoctoral training at the University of Michigan in the laboratory of Dr. Victor DiRita. Dr. Matson joined the Department of Medical Microbiology and Immunology in June of 2013.
Research group (left to right): Cara, DeAngelis (MMI Graduate Student); Jessica Saul (MMI Graduate Student); Yvette Unoarumhi (MS Student); Dr. Jyl Matson (Ph.D.); Laura Stanbery Nejedlik (Research Assistant); Sarah Plecha (Postdoctoral Fellow)
Current grant funding:
NIH R01. Identification of novel inhibitors of a Vibrio cholerae stress response pathway. (4/1/13-3/31/16)
Representative Publications:
(2017). Sterilization of Biofilm on a Titanium Surface Using a Combination of Nonthermal Plasma and Chlorhexidine Digluconate. BioMed Research International, 2017, 6085741. http://doi.org/10.1155/2017/6085741.
(2017). Assay development and high-throughput screening for small molecule inhibitors of a Vibrio cholerae stress response pathway. Drug Design, Development and Therapy, 11, 2777鈥�2785. http://doi.org/10.2147/DDDT.S144391.
(2017). A putative Vibrio cholerae two-component system controls a conserved periplasmic protein in response to the antimicrobial peptide polymyxin B. PLoS ONE, 12(10), e0186199. http://doi.org/10.1371/journal.pone.0186199.
(2016). Evolution of a global regulator: Lrp in four orders of 纬-Proteobacteria. BMC Evolutionary Biology, 16, 111. http://doi.org/10.1186/s12862-016-0685-1.
(2015), Regulated intramembrane proteolysis of the virulence activator TcpP in Vibrio cholerae is initiated by the tail-specific protease (Tsp). Molecular Microbiology, 97: 822鈥�831. doi:10.1111/mmi.13069.
(2015), Single-molecule tracking in live Vibrio cholerae reveals that ToxR recruits the membrane-bound virulence regulator TcpP to the toxT promoter. Molecular Microbiology, 96: 4鈥�13. doi:10.1111/mmi.12834.
(2014). Genome Sequence of Klebsiella pneumoniae Respiratory Isolate IA565. Genome Announcements, 2(5), e00896鈥�14. http://doi.org/10.1128/genomeA.00896-14.
(2014). Imaging Live Cells at the Nanometer-Scale with Single-Molecule Microscopy: Obstacles and Achievements in Experiment Optimization for Microbiology. Molecules (Basel, Switzerland), 19(8), 12116鈥�12149. http://doi.org/10.3390/molecules190812116.
(2014). "Genome Sequence of Klebsiella pneumoniae Urinary Tract Isolate Top52." Genome Announc. pii: e00668-14. doi: 10.1128/genomeA.00668-14.
. (2010). 鈥淧olymyxin B resistance in El Tor Vibrio cholerae requires lipid acylation catalyzed by MsbB.鈥� J. Bacteriol. 192:2044-2052.
. (2008). 鈥淟crG secretion is not required for blocking of Yops secretion in Yersinia pestis.鈥� BMC Microbiol. 8:29.
(2007). 鈥淩egulatory networks controlling Vibrio cholerae virulence gene expression.鈥� Infect. Immun. 75:5542-5549.
(2005). 鈥淒egradation of the membrane-localized virulence activator TcpP by the YaeL protease in Vibrio cholerae.鈥� Proc. Natl. Acad. Sci. USA. 102:16403-16408.
(2005). 鈥淚mmunization of mice with YscF provides protection from Yersinia pestis 颈苍蹿别肠迟颈辞苍蝉.鈥� BMC Microbiol. 5:38.
2002. 鈥淚nteraction of the Yersinia pestis type III regulatory proteins LcrG and LcrV occurs at a hydrophobic interface.鈥� BMC Microbiol. 2:16.
(2002). 鈥淕enome sequence of Yersinia pestis 碍滨惭.鈥� J. Bacteriol. 184:4601-4611.
(2001). 鈥淟crG-LcrV interaction is required for control of Yops secretion in Yersinia pestis.鈥� J. Bacteriol. 183:5082-5091.
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