Rice University
BioSciences at Rice

Charles Stewart

Professor of BioSciences

Infection of Bacillus subtilis by bacteriophage SPO1 causes profound changes in the genetic processes of the host cell. Stewart's Research Synthesis of host DNA, RNA, and protein is shut off, presumably to prevent those syntheses from competing with the corresponding phage biosyntheses for materials, energy, and access to biosynthetic machinery. Such global redirection of the cell's resources requires regulatory mechanisms of great sophistication and specificity, to eliminate the host-specific biosyntheses, while exactly the same processes, specific to the phage genome, proceed with enormous efficiency in the same cell. We are analyzing the mechanisms by which SPO1 accomplishes this takeover of the host cell. We have identified a cluster of 24 genes in the terminal redundancy of SPO1, which specifies most or all of the necessary machinery. By observing the effect of expression of each gene in uninfected cells, and the effect of mutational inactivation of each gene on the progress of infection, we are defining the specific roles of the 24 gene products. Activities that have been identified for specific gene products include: (1) shutoff of host DNA and RNA synthesis; (2) regulation of the timing of those shutoffs; (3) inhibition of host cell division; and (4) regulation of expression of the 24 genes. The broad spectrum bactericidal activity of some of these gene products makes them a potential basis for development of new antibiotics.

Infection of Bacillus subtilis by bacteriophage SPO1 causes profound changes in the genetic processes of the host cell. Stewart's ResearchSynthesis of host DNA, RNA, and protein is shut off, presumably to prevent those syntheses from competing with the corresponding phage biosyntheses for materials, energy, and access to biosynthetic machinery. Such global redirection of the cell's resources requires regulatory mechanisms of great sophistication and specificity, to eliminate the host-specific biosyntheses, while exactly the same processes, specific to the phage genome, proceed with enormous efficiency in the same cell. We are analyzing the mechanisms by which SPO1 accomplishes this takeover of the host cell. We have identified a cluster of 24 genes in the terminal redundancy of SPO1, which specifies most or all of the necessary machinery. By observing the effect of expression of each gene in uninfected cells, and the effect of mutational inactivation of each gene on the progress of infection, we are defining the specific roles of the 24 gene products. Activities that have been identified for specific gene products include: (1) shutoff of host DNA and RNA synthesis; (2) regulation of the timing of those shutoffs; (3) inhibition of host cell division; and (4) regulation of expression of the 24 genes. The broad spectrum bactericidal activity of some of these gene products makes them a potential basis for development of 

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Stewart, C. "Analysis of Host-takeover during SPO1 infection of Bacillus subtilis" in "Bacteriophages: Methods and Protocols", eds Clokie, M., Lavigne, R. and Kropinski, A. (submitted for publication, 2014).

Tevdoradze, E., Kvachadze, L., Kutateladze, M., and Stewart, C.R. Bactericidal genes of Staphylococcal bacteriophage Sb-1.  Current Microbiology, 68 2014: 204-210

Stewart, C. "Site-specific Mutagenesis of Bacillus subtilis phage SPO1" in "Bacteriophages: Methods and Protocols", eds Clokie, M., Lavigne, R. and Kropinski, A. (submitted for publication, 2014).

 

Stewart, C.R., Deery, W.J., Egan, E.S.K., Myles, B., and Petti, A. A. The product of SPO1 gene 56 inhibits host cell division during infection of Bacillus subtilis by bacteriophage SPO1.  Virology, 447 2013: 249-253

Stewart, C.R. et al. SPO1-like Viruses.  The Springer Index of Viruses, 2nd edition 2011 : 931-939

Stewart, C.R., Yip, T.K., Myles, B., Laughlin, L. Roles of genes 38, 39, and 40 in shutoff of host biosyntheses during infection of Bacillus subtilis by bacteriophage SPO1.  Virology, 392 2009: 271-274

Stewart, C.R., Casjens, S.R., Cresawn, S.G., Houtz, J.M., Smith, A.L., Ford, M.E., Peebles, C.L., Hatfull, G.F., Hendrix, R.W., Huang, W.M., Pedulla, M.I. The genome of Bacillus subtilis bacteriophage SPO1.  J. Mol. Biol., 388 2009: 48-70

Sampath, A., and Stewart, C. Roles of genes 44, 50, and 51 in regulating gene expression and host-takeover during infection of Bacillus subtilis by bacteriophage SPO1.  J. Bacteriology, 186 2004: 1785-1792

Stewart, C.R. Bacteriophage SPO1.  in Encyclopedia of Virology, 2nd Edition (Webster, R.G., and Granoff, A., eds.) 1999: 1681-1685

Stewart, C.R., Gaslightwala, I., Hinata, K., Krolikowski, K.A., Needleman, D.S., Peng, A.S.-Y., Peterman, M.A., Tobias, A., and Wei, P. Genes and Regulatory Sites of the 'Host Takeover Module' in the Terminal Redundancy of Bacillus subtilis Bacteriophage SPO1.  Virology, 246 1998: 329-340

Wei, P., and Stewart, C.R. Genes that Protect Against the Host-Killing Activity of the E3 Protein of Bacillus subtilis Bacteriophage SPO1.  J. Bacteriol., 177 1995: 2933-2937

Wei, P., and Stewart, C.R. A Cytotoxic Early Gene of Bacillus subtilis Bacteriophage SPO1.  J. Bacteriol., 175 1993: 7887-7900

Stewart, C.R. SPO1 and Related Bacteriophases.  Bacillus subtilis and Other Gram-Positive Bacteria 1993: 813-829

Stewart, C.R. Bacteriophage SPO1.  Bacteriophages, Vol. I 1988: 477-515

Curran, J.F., and Stewart, C.R. Cloning and Mapping of the SPO1 Genome.  Virology, 142 1985: 78-97

Curran, J.F., and Stewart, C.R. Transcription of B. subtilis Plasmid pBD64, and Expression of Bacteriophage SPO1 Genes Cloned Therein.  Virology, 142 1985: 98-111

Stewart, C.R. Dissection of HA20, a Double Mutant of Bacteriophage SPO1.  J. Virol., 49 1984: 300-301

Curran, J.F., and Stewart, C.R. Recombination and Expression of a Cloned Fragment of the DNA of Bacillus subtilis Bacteriophage SPO1.  Virology, 120 1982: 307-317

Stewart, C.R., and Franck, M. Limited role of parental DNA in replication during infection by Bacillus subtilis phage SP01.  Virology, 110 1981: 221-224

Stewart, C.R., and Franck, M. Predominance of bacteriophage SP82 over bacteriophage SP01 in mixed infections of Bacillus subtilis.  J. Virol., 38 1981: 1081-1083

Cregg, J.M., and Stewart, C.R. EcoRI cleavage of DNA from phage SP01.  Virology, 85 1978: 601-605

Cregg, J.M., and Stewart, C.R. Terminal Redundancy of "High Frequency of Recombination" Markers of Bacillus subtilis Phage SP01.  Virology, 86 1978: 530-541

Glassberg, J.S., Franck, M., and Stewart, C.R. Initiation and Termination Mutants of Bacillus subtilis phage SP01.  J. Virol., 21 1977: 147-152

Glassberg, J.S., Franck, M., and Stewart, C.R. Multiple Origins of Replication for Bacteriophage SP01.  Virology, 78 1977: 433-441

Cregg, J.M., and Stewart, C.R. Timing of Initiation of DNA Replication in SP01 Infection of Bacillus subtilis.  Virology, 80 1977: 289-296

Stewart, C.R., Click, B., and Tole, M.F. DNA Replication and Late Protein Synthesis during SP82 Infection of Bacillus subtilis.  Virology, 50 1972: 653-663

Stewart, C.R., Cater, M., and Click, B. Lysis of Bacillus subtilis by bacteriophage SP82 in the absence of DNA synthesis.  Virology, 46 1971: 327-336

Stewart Lab

  • B.S. Zoology (1962) University of Wisconsin
  • Ph.D. Genetics (1967) Stanford University
  • Institute of Biosciences and Bioengineering
Research Areas
  • Molecular Genetics. Microbial Biotechnology. Bacteriophage biology.
Professional Experience
  • American Cancer Society Postdoctoral Fellow
    Albert Einstein College of Medicine
    1967-1969
  • Assistant Professor
    Rice University
    1969-1974
  • Associate Professor
    Rice University
    1974-1981
  • Professor
    Rice University
    1981-1989
  • Professor
    Rice University
    1989-present
Contact Information
Email: crs@rice.edu
Phone: 713-348-4926
Office: George R. Brown Hall, W104