James M. Musser, M.D., Ph.D.

Baylor College of Medicine, Building: BCM-Smith Medical Research Bld
Room: BCMS-S234A
Phone: 713.798.3823
E~mail: musser@bcm.tmc.edu

RESEARCH INTERESTS:

The long-term goals of research conducted in my laboratory are to understand the molecular basis of diseases caused by the human pathogenic bacterium Group A Streptococcus (GAS) and elucidate the molecular basis underlying variation in the character of disease caused by Mycobacterium tuberculosis. Genome-scale and high-throughput strategies are used to investigate: (1) the role of extracellular GAS proteins in host-pathogen interactions (2) potential immunoprophylaxis applications of these proteins (3) the molecular pathogenesis of rheumatic fever and rheumatic heart disease. In M. tuberculosis, the laboratory is addressing: (1) the genetics of disease specificity recently identified for certain M. tuberculosis clones and (2) the human genetics of susceptibility to this pathogen. A highly integrated approach is used that encompasses bacterial molecular genetics, genome sequencing, expression microarray, molecular population genetic analysis, and human genetic epidemiology.

Selected Publications

Smoot J.C, Barbian K.D, Van Gompel J.J, Smoot L.M, Chaussee M.S, Sylva G.L, Sturdevant D.E, Ricklefs S.M, Porcella S.F, Parkins L.D, Beres S.B, Campbell D.S, Smith T.M, Zhang Q, Kapur V, Daly J.A, Veasy L.G, and Musser J.M. 2002. Genome sequence and comparative microarray analysis of serotype M18 group A Streptococcus strains associated with acute rheumatic fever outbreaks. Proc. Natl. Acad. Sci.USA 99:4668-4673.

Voyich JM, Sturdevant DE, Braughton KR, Kobayashi SD, Lei B, Virtaneva K, Dorward DW, Musser JM, DeLeo FR. 2003. Genome-wide protective response used by group A Streptococcus to evade destruction by human polymorphonuclear leukocytes. Proc Natl Acad Sci USA 100:1996-2001.

Hoe N.P, Ireland R.M, DeLeo F.R, Gowen B.B, Dorward D.W, Voyich J.M, Liu M, Burns E.H Jr, Culnan D.M, Bretscher A, and Musser J.M. 2002. Insight into the molecular basis of pathogen abundance: group A Streptococcus inhibitor of complement inhibits bacterial adherence and internalization into human cells. Proc. Natl. Acad. Sci. USA 99:7646-7651.

Beres S.B, Sylva G.L, Barbian K.D, Lei B, Hoff J.S, Mammarella N.D, Liu M.Y, Smoot J.C, Porcella S.F, Parkins L.D, Campbell D.S, Smith T.M, McCormick J.K, Leung D.Y, Schlievert P.M, and Musser J.M. 2002. Genome sequence of a serotype M3 strain of group A Streptococcus: phage-encoded toxins, the high-virulence phenotype, and clone emergence. Proc. Natl. Acad. Sci. USA 99:10078-10083.

Graham M.R, Smoot L.M, Migliaccio C.A, Virtaneva K, Sturdevant D.E, Porcella S.F, Federle M.J, Adams G.J, Scott J.R, and Musser J.M. 2002. Virulence control in group A Streptococcus by a two-component gene regulatory system: global expression profiling and in vivo infection modeling. Proc. Natl. Acad. Sci. USA 99:13855-13860.

Gutacker M.M, Smoot J.C, Migliaccio C.A, Ricklefs S.M, Hua S, Cousins D.V, Graviss E.A, Shashkina E, Kreiswirth B.N, and Musser J.M. 2002. Genome-wide analysis of synonymous single nucleotide polymorphisms in Mycobacterium tuberculosis complex organisms. Resolution of genetic relationships among closely related microbial strains. Genetics 162:1533-1543.