Abstract

The mechanisms by which new pathogens human pathogens emerge are of increasing relevance in the control of infectious diseases. My long-term research goal is to explore the role of biofilms in the emergence of new pathogenic strains. Vibrio cholerae O139, a recently emerged pathogenic strain, will be used as a model for this study. V. cholerae is an inhabitant of marine environments. Although biofilm formation is an integral part of its existence in this environment, little is known about the V. cholerae biofilm at the molecular level. A rapid screen for biofilm formation will be used to isolate V. cholerae O139 transposon insertion mutants that are unable to initiate and maintain biofilms. The mutants will be characterized at the molecular biological, microscopic, and molecular levels. Genes involved in biofilm formation that are unique to V. cholerae O139 among the pathogenic V. cholerae strains will be identified and studied to determine possible methods of horizontal gene transfer.
My specific aims are to: (I) Isolate and characterize V. cholerae O139 mutants that are defective in initiation of biofilm formation, (II) Identify and characterize genes responsible for the maintenance of V. cholerae O139 biofilms, and (III) Identify genes involved in biofilm formation that are unique to V. cholerae O139.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08AI001588-02
Application #
6149734
Study Section
Microbiology and Infectious Diseases B Subcommittee (MID)
Project Start
1999-02-15
Project End
2000-08-07
Budget Start
2000-02-01
Budget End
2000-08-07
Support Year
2
Fiscal Year
2000
Total Cost
$52,828
Indirect Cost

  Institution

Name
Massachusetts General Hospital
Department
Type
DUNS #
073130411
City
Boston
State
MA
Country
United States
Zip Code
02199

  Publications

Watnick, P I; Lauriano, C M; Klose, K E et al. (2001) The absence of a flagellum leads to altered colony morphology, biofilm development and virulence in Vibrio cholerae O139. Mol Microbiol 39:223-35
Watnick, P I; Kolter, R (1999) Steps in the development of a Vibrio cholerae El Tor biofilm. Mol Microbiol 34:586-95
Chou, J; Roizman, B (1992) The gamma 1(34.5) gene of herpes simplex virus 1 precludes neuroblastoma cells from triggering total shutoff of protein synthesis characteristic of programed cell death in neuronal cells. Proc Natl Acad Sci U S A 89:3266-70
Roller, R J; Roizman, B (1992) The herpes simplex virus 1 RNA binding protein US11 is a virion component and associates with ribosomal 60S subunits. J Virol 66:3624-32
Romanelli, M G; Mavromara-Nazos, P; Spector, D et al. (1992) Mutational analysis of the ICP4 binding sites in the 5' transcribed noncoding domains of the herpes simplex virus 1 UL 49.5 gamma 2 gene. J Virol 66:4855-63
McCormick, L; Roller, R J; Roizman, B (1992) Characterization of a herpes simplex virus sequence which binds a cellular protein as either a single-stranded or double-stranded DNA or RNA. J Virol 66:3435-47
Baines, J D; Roizman, B (1992) The UL11 gene of herpes simplex virus 1 encodes a function that facilitates nucleocapsid envelopment and egress from cells. J Virol 66:5168-74
Barker, D E; Roizman, B (1992) The unique sequence of the herpes simplex virus 1 L component contains an additional translated open reading frame designated UL49.5. J Virol 66:562-6
Liu, F; Roizman, B (1992) Differentiation of multiple domains in the herpes simplex virus 1 protease encoded by the UL26 gene. Proc Natl Acad Sci U S A 89:2076-80
Baines, J D; Roizman, B (1992) The cDNA of UL15, a highly conserved herpes simplex virus 1 gene, effectively replaces the two exons of the wild-type virus. J Virol 66:5621-6

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