Howard, Susan, Ph.D.

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Contact: susan.howard@uthct.edu

Education:
Ph.D., Division of Virology, Dept. of Pathology, University of Cambridge, U.K., 1992.
M. Sc., Dept. of Biological Sciences, University of Windsor, Ontario, Canada, 1987.
B.Sc., (Honours, Microbiology), University of Windsor, 1984.

Research Interest:
Investigating the regulation of gene expression in mycobacteria.

Current Projects:

1. Characterization of transcription factors and regulatory networks that govern the response of Mycobacterium tuberculosis to stress conditions.
2. Identification of regulatory elements that control changes in colony morphology in Mycobacterium abscessus.

Research Overview:
The spread of Mycobacterium tuberculosis, the causative agent of tuberculosis, has resulted in a tremendous global burden of illness and mortality. The ability of this bacteria to survive and multiply in human macrophages ("white blood cells"), has made M. tuberculosis a highly successful pathogen. Because macrophages are designed to engulf and destroy bacteria, their internal environment is highly damaging to bacteria. M. tuberculosis has developed methods to survive this stressful environment. Our research focuses on determining how M. tuberculosis regulates its response to stressful conditions such as those found within macrophages.

We are also studying M. abscessus, an environmental organism which can infect cystic fibrosis patients. M. abscessus can form rough or smooth colonies, and an ability to switch between these different colony types may influence survival and spread of the organism in human tissues.

Selected Papers and Abstracts:

• Howard ST, Rhoades E, Recht J, Alsup A, Pang X, Kolter R, Lyons CR, Byrd TF. 2006. Spontaneous reversion of Mycobacterium abscessus from a smooth to a rough morphotype is associated with reduced expression of glycopeptidolipid and reacquisition of an invasive phenotype. Microbiology 2006 Jun;152(Pt 6):1581-90.
• Samten B, Howard ST, Weis SE, Wu S, Shams H, Safi H, and Barnes PF. 2005. Cyclic AMP response element-binding protein positively regulates production of IFN-gamma by T cells in response to a microbial pathogen. Journal of Immunology 174:6357-6363.
• Safi H, Barnes PF, Lakey DL, Shams H, Samten B, Vankayalapati R, Howard ST. 2004. IS 6110 functions as a mobile, monocyte-activated promoter in Mycobacterium tuberculosis. Mol. Micro. 52:999-1012.
• Talaat AM, Lyons CR, Howard ST, Johnston SA. 2004. The temporal expression profile of Mycobacterium tuberculosis in mice. Proc. Natl. Acad. Sci. 101:4602-4607.
• Wu S, Howard ST, Lakey DL, Kipnis A, Samten B, Safi H, Gruppo V, Wizel B, Shams H, Basaraba RJ, Orme IM, Barnes PF. 2004. The principal sigma factor sigA mediates enhanced growth of Mycobacterium tuberculosis strains in vivo. Mol. Micro. 51:1551-1562.
• Talaat AM, Howard ST, Hale W. 4th, Lyons R, Garner H, Johnston SA. Genomic DNA standards for gene expression profiling in Mycobacterium tuberculosis. Nucleic Acids Res 2002 Oct 15;30(20):e104.
• Howard ST, Byrd TF, Lyons CR. A polymorphic region in Mycobacterium abscessus contains a novel insertion sequence element. Microbiology 2000;148:2987-2986.
• Howard ST and Byrd TF. The rapidly-growing mycobacteria: saprophytes and parasites. Microbes and Infection 2000;2:1845-1853.
• Howard ST, Ray CA, Patel DD, Antczak JB, Pickup DJ. A 43-nucleotide RNA cis-acting element governs the site-specific formation of the 3’ end of a poxvirus late mRNA. Virology 1999;255:190-204.
• Howard ST, Oughton MT, Haddad A, Johnson W. Absence of the genetic marker IS6110 from a strain of Mycobacterium tuberculosis isolated in Ontario. Can J Infect Dis 1998;9:48-53.