Martin, Daniel

member of

Microbiology and Immunology Research Associate Professor

selected publications

academic article
- Characterization of the organic hydroperoxide resistance system of Brucella abortus 2308. Journal of Bacteriology. 194:5065-5072. 2012
- SodA is a major metabolic antioxidant in Brucella abortus 2308 that plays a significant, but limited, role in the virulence of this strain in the mouse model. Microbiology. 158:1767-1774. 2012
- Survival of the fittest: How Brucella strains adapt to their intracellular niche in the host. Medical Microbiology and Immunology. 198:221-238. 2009
- The manganese transporter MntH is a critical virulence determinant for Brucella abortus 2308 in experimentally infected mice. Infection and Immunity. 77:3466-3474. 2009
- Invasion and intracellular survival of Burkholderia cepacia. Infection and Immunity. 68:24-29. 2000
- Erratum: Invasion and intracellular survival of Burkholderia cepacia (Infection and Immunity (2000) 68:1 (24-29)). Infection and Immunity. 68:3792. 2000
- Analysis of promoters controlled by the putative sigma factor AlgU regulating conversion to mucoidy in Pseudomonas aeruginosa: Relationship to Ïƒ(E) and stress response. Journal of Bacteriology. 176:6688-6696. 1994
- Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: Environmental stress and regulation of bacterial virulence by alternative sigma factors. Journal of Bacteriology. 176:2773-2780. 1994
- Gene cluster controlling conversion to alginate-overproducing phenotype in Pseudomonas aeruginosa: Functional analysis in a heterologous host and role in the instability of mucoidy. Journal of Bacteriology. 176:3375-3382. 1994
- Conversion to mucoidy in Pseudomonas aeruginosa. Bio/Technology. 11:1133-1136. 1993
- The algD promoter: Regulation of alginate production by Pseudomonas aeruginosa in cystic fibrosis. Cellular and Molecular Biology Research. 39:371-376. 1993
- Mechanism of conversion to mucoidy in Pseudomonas aeruginosa infecting cystic fibrosis patients. Proceedings of the National Academy of Sciences of the United States of America. 90:8377-8381. 1993
- Differentiation of Pseudomonas aeruginosa into the alginate-producing form: Inactivation of mucB causes conversion to mucoidy. Molecular Microbiology. 9:497-506. 1993
- Characterization of a locus determining the mucoid status of Pseudomonas aeruginosa: AlgU shows sequence similarities with a Bacillus sigma factor. Journal of Bacteriology. 175:1153-1164. 1993
- Mucoid Pseudomonas aeruginosa and cystic fibrosis: The role of mutations in muc loci. FEMS Microbiology Letters. 100:323-329. 1992
- Mucoid Pseudomonas aeruginosa in cystic fibrosis: Signal transduction and histone-like elements in the regulation of bacterial virulence. Molecular Microbiology. 5:1577-1583. 1991
- Role of the far-upstream sites of the algD promoter and the algR and rpoN genes in environmental modulation of mucoidy in Pseudomonas aeruginosa. Journal of Bacteriology. 172:6576-6580. 1990
- Mucoid Pseudomonas aeruginosa in cystic fibrosis: Mutations in the muc loci affect transcription of the algR and algD genes in response to environmental stimuli. Molecular Microbiology. 4:189-196. 1990
- Common denominators of promoter control in Pseudomonas and other bacteria. Bio/Technology. 7:1249-1254. 1989

research overview

Legionella pneumophila is a facultative intracellular pathogen and the causative agent of Legionnaires’ disease, a potentially fatal pneumonia. In the human lung, L. pneumophila invades and replicates within the pulmonary macrophages. Protozoa, which harbor the bacteria within contaminated water systems, are a significant reservoir of infection that have been linked to outbreaks of disease. The interaction of L. pneumophila with both amoebae, the protozoa most commonly associated with L. pneumophila, and macrophages is very similar. Following uptake, L. pneumophila alters vesicular trafficking to avoid phagosome-lysosome fusion and to subvert the bactericidal capabilities of the host cell. Replication within the host cell continues until the cell dies and releases the bacteria, which then initiate additional rounds of infection. My laboratory is currently studying genes activated during the intracellular growth of L. pneumophila in Acanthaboeba castellanii, a protozoan host, and in human macrophages. We expect these genes to be the best candidates for virulence determinants. Like most bacterial pathogens, L. pneumophila carefully regulates the expression of virulence. Previous studies have found that growth within amoebae enhanced the virulence of L. pneumophila. This phenotypic change in virulence was mirrored by changes in morphology, physiology, and gene expression. In order to identify genes that are activated within host cells we have utilized a promoter trapping technique known as differential fluorescence induction (DFI). This technology employs fluorescence activated cell sorting to select clones that are activated during infection of host cells from a random L. pneumophila promoter library fused to the green fluorescent protein. Using DFI, we have isolated a collection of genes that are specifically activated during infection of the host cell. This includes several novel genes that may contribute to virulence. Current and future studies are aimed at the complete molecular characterization of each gene, which will allow us to better understand the adaptation of L. pneumophila to this unique environment. This will include: (i) promoter mapping; (ii) identification of specific environmental cues necessary for regulation of the individual genes; (iii) identification and analysis of regulatory elements; and (iv) mutational analysis of individual genes to access their contribution to virulence in different models of infection. The results from these studies will give us insight into the contributions that these genes make to the host-pathogen interaction and may lead to new strategies for improved treatment and prevention of Legionnaires’ disease in humans.

education and training

Ph.D. in Microbiology and Immunology, University of Texas Health Science Center at San Antonio 1994
M.S. in Interdisciplinary Studies, University of Texas at Tyler , Biology, Chemistry, and Computer Science 1988

full name

Daniel Wynn Martin

mailing address

ECU, Brody School of Medicine, Dept of Microbiology and Immunology

Biotechnology Bldg. Rm. 120

Greenville, NC 27834

USA

geographic location

Health Sciences

fax

(252) 744-3535

VIVO @ East Carolina University

VIVO @ East Carolina University

Martin, Daniel Associate Professor

Positions

Affiliation

member of

Publications

selected publications

academic article

Research

research overview

Background

education and training

Contact

full name

mailing address

geographic location

fax