Jyl S. Matson, Ph.D.
Assistant Professor Vibrio cholerae stress response mechanisms and pathogenesis
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’s research is using next generation sequencing (RNAseq) to uncover new knowledge about how bacteria respond to various stressors. Our lab is particularly interested in using RNAseq to determine the function of previously uncharacterized V. cholerae proteins. 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.
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.
Current grant funding:
NIH R01. Identification of novel inhibitors of a Vibrio cholerae stress response pathway. (4/1/13-3/31/16)
Matson JS, Yoo HJ, Hakansson K, and DiRita VJ. 2010. “Polymyxin B resistance in El Tor Vibrio cholerae requires lipid acylation catalyzed by MsbB.” J. Bacteriol. 192:2044-2052.
Reina LD, O’Bryant DM, Matson JS and Nilles ML. 2008. “LcrG secretion is not required for blocking of Yops secretion in Yersinia pestis.” BMC Microbiol. 8:29.
Matson JS, Withey JH, and DiRita VJ. 2007. “Regulatory networks controlling Vibrio cholerae virulence gene expression.” Infect. Immun. 75:5542-5549.
Matson JS and DiRita VJ. 2005. “Degradation of the membrane-localized virulence activator TcpP by the YaeL protease in Vibrio cholerae.” Proc. Natl. Acad. Sci. USA. 102:16403-16408.
Matson JS, Durick KA, Bradley DS, and Nilles ML. 2005. “Immunization of mice with YscF provides protection from Yersinia pestis infections.” BMC Microbiol. 5:38.
Matson JS and Nilles ML. 2002. “Interaction of the Yersinia pestis type III regulatory proteins LcrG and LcrV occurs at a hydrophobic interface.” BMC Microbiol. 2:16.
Deng W, Burland V, Plunkett 3rd G, Boutin A, Mayhew GF, Liss P, Perna NT, Rose DJ, Mau B, Zhou S, Schwartz DC, Featherston JD, Lindler LE, Brubaker RR, Plano GV, Straley SC, McDonough KA, Nilles ML, Matson JS, Blattner FR, and Perry RD. 2002. “Genome sequence of Yersinia pestis KIM.” J. Bacteriol. 184:4601-4611.
Matson JS and Nilles ML. 2001. “LcrG-LcrV interaction is required for control of Yops secretion in Yersinia pestis.” J. Bacteriol. 183:5082-5091.