Tung Hoang

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Tung received his B.Sc. in Biochemistry from the University of Calgary, Canada, in 1994. He earned a thesis-based M.Sc. degree in Microbiology and Infectious Diseases at the University of Calgary in 1996. After working for 1 year, we entered the Ph.D. program at Colorado State University, specializing in Bacterial Genetics, and earned his Ph.D. 3 years later in early 2000. He published 13 papers after his Ph.D. and received 2 years of postdoctoral fellowship support from the Natural Sciences and Engineering Research Council of Canada, the Alberta Heritage Foundation for Medical Research, and Minister of Fisheries and Oceans of Canada. He joined the faculty in the Department of Microbiology at UHM, as an Assistant Professor, in the fall of 2002. Tung is now a Full Professor in this department.

Hobbies and extracurricular activities – He enjoys aquaponic, badminton, running, and fishing. With help from wonderful neighbors, he has started a small tropical fruit tree orchard, including trees of several citruses, avocado, banana, breadfruit, durian, fig, guava, jackfruit, langsat, longan, lychee, mango, mangosteen, mountain-apple, rambutan, papaya, pomelo, sapote (chico), sugarcane, star-apple, star-fruit, wi-apple.

Snyder 308D

Courses Taught


Micr 470 Microbial Pathogenesis
Micr 470 Microbial Pathogenesis Lab
Micr 499 Microbiological Problems
Micr 685 Molecular-Cellular Pathogens
Micr 695 Research Literature Review
Micr 699 Directed Research
Micr 700 Thesis Research
Micr 800 Dissertation Research


Micr 351 Biology of Microorganisms
Micr 351L Biology of Microorganisms Lab
Micr 470 Bacterial Pathogenesis
Micr 470 Microbial Pathogenesis Lab
Micr 499 Microbiological Problems
Micr 695 Research Literature Review
Micr 699 Directed Research
Micr 700 Thesis Research
Micr 800 Dissertation Research

Research Interests

  • Functional Genomics of Single- and Mixed-species Biofilms in Spatiotemporal Scales
  • Characterization of Mutations in Unknown Genes Expressed in the Burkholderia pseudomallei transitome

Current Research

The Hoang Lab currently has two areas of infectious disease research interests, focusing on the genetics and pathophysiology of i) Burkholderia pseudomallei and ii) Pseudomonas aeruginosa

i) B. pseudomallei is a CDC category B and potential bioterrorism agent, causing a disease called melioidosis throughout the tropical regions mainly in Southeast Asia and Northern Australia. The disease resembles and can be misdiagnosed for tuberculosis. This bacterium can often be isolated from the water and soil of rice fields (panel A) and other environments throughout the tropical regions. The organism can be aerosolized and mortality rates of infected patients can be as high as 50-90%; thus, precautions to prevent inhalation in the laboratory are necessary (panel B and C).

The lab currently researches the molecular pathogenesis of B. pseudomallei during its infection within host-cells. Our hypothesis is that B. pseudomallei, as it encounters and senses uniquely different intracellular environments and performs sequential steps in the infection process, will undergo differential gene expression at each stage of intracellular cycle. We pioneered and studied global transcriptional profiling of single B. pseudomallei cells as it transit through the host cell, which we cumulatively named a “transitome.” Our goal is to more clearly identify the genes, and hence the proteins, required for eukaryotic hosts’ cellular infection in each spatially defined infectious stage (vesicle, cytoplasm, and membrane protrusion; panels E-H). Ultimately, understanding the function of these virulence genes and mechanisms of infection and disease at the molecular level will aid in rational drug and vaccine design.

The lab also has pioneered, successfully tested, and published several molecular genetic tools, aiding molecular genetic studies in B. pseudomallei and other Burkholderia species. The ease of genetic manipulations of B. pseudomallei using these tools will expand research that will contribute to molecular genetics, pathogenesis, and bacteria-host interaction studies crucial for the discovery of novel vaccines, therapeutics, and diagnostic targets.

Panel A - Rice fields
Panel A - Rice fields
Panel B - Laboratory
Panel B - Laboratory
Panel C - Laboratory
Panel C - Laboratory

ii) P. aeruginosa is an opportunistic pathogen of plants, animals, and humans. The major focus of this second research topic in the lab involves P. aeruginosa in Cystic Fibrosis (CF) lung infection. P. aeruginosa has the ability to obtain nutrients in the CF lung for high-cell-density (HCD) replication (>109 cfu/mL of sputum), leading to quorum-sensing controlled virulence expression. The long-term goal is to define the metabolic capability of P. aeruginosa within the CF lung and the host pulmonary nutrient factors that contribute to HCD replication. Our hypothesis is that P. aeruginosa utilizes surfactant lipids as one of the available nutrient and energy sources, affording replication and maintenance at HCD. The rationale is that knowledge of the pathophysiology of P. aeruginosa, contributing to lung surfactant lipid degradation for HCD replication, would lead to innovative approaches for improved treatment extending the lives of CF patients who suffer from debilitating and fatal chronic lung infections.

Lung surfactant components (90% lipids and 10% proteins), especially lipids, are absolutely essential for normal pulmonary function. Of the 90% lipids in lung surfactant, 80% is phosphatidylcholine (PC). The lipid component of lung surfactant (i.e., PC) is readily metabolized by P. aeruginosa in vitro. Phospholipases and lipases, required for PC degradation, are essential virulence determinants expressed in vivo to degrade PC into three constituents (fatty acid, glycerol, and phosphorylcholine). All three constituents are also readily metabolized by P. aeruginosa in vitro. The metabolism of glycerol and phosphorylcholine is fairly well characterized. However, the pathways through which fatty acid (FA) constituents of PC are further metabolized by P. aeruginosa are undefined. The research in the lab currently focuses on establishing the importance of FA degradation pathways of P. aeruginosa and their contributions to bacterial in vivo replication.

Selected Publications

NCBI Publications

  1. Kang Y., McMillan I.A., Norris M.H., and Hoang, T. T. Single prokaryotic cell isolation and total transcript amplification protocol for transcriptomic analysis. Under consideration in Nature Protocols 10(7): 974-984.
  2. Sun Z., Kang Y., Norris M.H., Troyer R.M., Son M.S., Schweizer H.P., Dow S.W., Hoang T.T. 2014. Blocking phosphatidylcholine utilization in Pseudomonas aeruginosa, via mutagenesis of fatty acid, glycerol and choline degradation pathways, confirms the importance of this nutrient source in vivo. PLoS ONE 9(7): e0103778 [PMCID: PMC4113454].
  3. Zarzycki-Siek, J., Norris, M.H., Kang, Y., Sun, Z., Bluhm, A.P., McMillan, I.A., Hoang, T.T. 2013. Elucidating the Pseudomonas aeruginosa fatty acid degradation pathway: identification of additional fatty acyl-CoA synthetase homologues. PLoS ONE 8(5): e0064554 [PMCID: PMC3667196].
  4. Norris, M.H., Propst, K.L., Kang, , K., Dow, S.W., Schweizer, H.P., and Hoang, T.T. 2011. The Burkholderia pseudomalleiasd mutant exhibits attenuated intracellular infectivity and imparts protection against acute inhalation melioidosis in mice. Infection and Immunity 79(10):4010-4018 [PMCID: PMC3187240].
  5. Kang, Y., Norris, M., Zarzycki-Siek, J., Donachie, S.P., Nierman, W.C., and Hoang, T.T. 2011. Transcript amplification from single bacterium for transcriptome analysis. Genome Research 21: 925-935. [PMCID:PMC3106325].
  6. Kang, Y., Norris, M., Wilcox, B.A., Tuanyok, A., Keim, P.S., and Hoang, T.T. 2011. Knockout and pullout recombineering for naturally transformable Burkholderia thailandensis and Burkholderia pseudomallei. Nature Protocols 6(8): 1085-1104. [PMCID:PMC3564556].
  7. Norris MH, Kang Y, Wilcox B, Hoang TT. 2010. Stable site-specific fluorescent tagging constructs optimized for Burkholderia species. Applied Environmental Microbiology 76(22):763540. [PMCID:PMC2976199].
  8. Kang Y, Zarzycki-Siek J, Walton CB, Norris MH, Hoang TT. 2010. Multiple FadD acyl-CoA synthetases contribute to differential fatty acid degradation and virulence in Pseudomonas aeruginosa. PLoS ONE 5(10):e13557. [PMCID:PMC2958839].
  9. Norris, M.H., Kang, Y., Lu, D., Wilcox, B.A., and Hoang T.T. 2009. Glyphosate Resistance as a Novel Select-Agent-Compliant Non-Antibiotic Selectable Marker in Chromosomal Mutagenesis of the Essential Genes asd and dapB of Burkholderia pseudomallei . Applied and Environmental Microbiology 75(19):6062-6075. [PMCID:PMC2753064].
  10. Kang, Y., Lunin, V.V., Skarina, T., J., Savchenko, A., Schurr, M.J., and Hoang, T.T. 2009. The long-chain fatty acid sensor, PsrA, modulate the expression of rpoS and the type III secretion exsCEBA-operon in Pseudomonas aeruginosa. Molecular Microbiology 73(1):120-136. [PMCID:PMC2759274].
  11. Kang, Y., Norris, M.H., Barrett, A.R., Wilcox, B.A. and Hoang, T.T. 2009. Engineering of tellurite-resistant genetic tools for single-copy chromosomal analysis of Burkholderia spp. and characterization of the B. thailandensis betBA-operon. Applied and Environmental Microbiology 75(12):4015-4027. [PMCID:PMC2698364].
  12. Barrett, R.B., Kang, Y., Inamasu, K.S., Son, M.S., Vukovich, J.M., and T.T. Hoang. 2008. Genetic tools for allelic-replacement in Burkholderia species. Applied and Environmental Microbiology 74(14):4498-4508. [PMCID:PMC2493169].
  13. Kang, Y., D. T. Nguyen, M. S. Son, and T. T. Hoang. 2008. The Pseudomonas aeruginosa PsrA responds to long-chain fatty acid signals to regulate the fadBA5 ß-oxidation operon. Microbiology 145(6):1584-1596.
  14. Son, S.S., Nguyen, D.T., Kang, Y., and T.T. Hoang. 2008. Engineering of FRT-lacZ fusion constructs: induction of the Pseudomonas aeruginosa fadAB1 operon by medium and long chain-length fatty acids. Plasmid 59(2):111-118.
  15. Son, M.S., Matthews Jr., W.J., Kang, Y. Nguyen, D.T., and T.T. Hoang. 2007. In vivo evidence of Pseudomonas aeruginosa nutrient acquisition and pathogenesis in the lungs of cystic fibrosis patients. Infection and Immunity 75(11):5313-5324.
  16. Kang, Y., Son, M.S., and T.T. Hoang. 2007. One step engineering of T7-expression strains for protein production: increasing the host-range of T7-expression system. Protein Expression and Purification 55: 325-333.
  17. Yamniuk, A.P., Nguyen, L.T., Hoang, T.T., and Vogel, H.J. 2004. Metal ion binding properties and conformational states of calcium- and integrin-binding protein. Biochemistry 43: 2558-2568.
  18. Hoang, T.T., S.A. Sullivan, J.K. Cusick and H.P. Schweizer. 2002. ß-ketoacyl acyl carrier protein reductase (FabG) activity of the fatty acid biosynthetic pathway is a determining factor of 3-oxo-homoserine lactone acyl chain lengths. Microbiology 148: 3849-3856.
  19. Habash, M.B., Beaudette, L.A., Cassidy, M.B., Leung, K.T., Hoang, T., Vogel, H.J., Trevors, J.T., and H. Lee. 2002. Characterization of tetrachlorohydroquinone reductive dehalogenase from Sphingomonas sp. UG30. Biochemical & Biophysical Research Communications 299:634-640.
  20. Hoang, T.T., Kutchma, A.J., Becher, A., and Schweizer, H.P. 2000. A site-specific gene integration system for Pseudomonas aeruginosa. Plasmid 43: 59-72.
  21. Barekzi, N., Beinlich, K.L., Hoang, T.T., Pham, X.-Q., Karkhoff-Schweizer, R.R., and H.P. Schweizer. 2000. The oriC-containing region of the Pseudomonas aeruginosa chromosome undergoes large inversions at high frequency. Journal of Bacteriology 182:7070-7074.
  22. Rungtip, C., Beinlich, K., Hoang, T.T., Becher, A., Karkhoff-Schweizer, R.R., Schweizer, H.P. 2000. Cross-Resistance between Triclosan and Antibiotics in Pseudomonas aeruginosa is Mediated by Multidrug Efflux Pumps: Exposure of a Susceptible Mutant Strain to Triclosan Selects nfxB Mutants Overexpressing MexCD-OprJ. Antimicrobial Agents and Chemotherapy 45(2): 428-432.
  23. Kutchma, A.J., Hoang, T.T., and Schweizer, H.P. 1999. Characterization of a Pseudomonas aeruginosa fatty acid biosynthetic gene cluster: purification of acyl carrier protein (ACP) and malonyl-CoA:ACP transacylase (FadD). Journal of Bacteriology 181: 5498-5504.
  24. Hoang, T.T., and Schweizer, H.P. 1999. Characterization of Pseudomonas aeruginosa enoyl-acyl carrier protein reductase (FabI): a target for the antimicrobial triclosan and its role in acylated homoserine lactone synthesis. Journal of Bacteriology 181: 5489-5497.
  25. Hoang, T.T., YuFang Ma, Stern, R.J., McNeil, M.R., and Schweizer, H.P. 1999. Construction and use of low-copy number T7 expression vectors for purification of problem proteins: purification of Mycobacterium tuberculosis RmlD and Pseudomonas aeruginosa LasI and RhlI proteins, and functional analysis of purified RhlI. Gene 237: 361-371.
  26. Hoang, T.T., Karkhoff-Schweizer, R.R., Kutchma, A.J., and Schweizer, H.P. 1998. A broad-host-range Flp-FRT recombination system for site-specific excision of chromosomally-located DNA sequences: application for isolation of unmarked Pseudomonas aeruginosa mutants. Gene 212: 77-86.
  27. Handfield, M., Schweizer, H.P., Mahan, M.J., Sanschargrin, F., Hoang, T.T, and Levesque, R.C. 1998. Asd-GFP vectors for in vivo expression technology in Pseudomonas aeruginosa and other Gram-negative bacteria. BioTechniques 24(2): 261-264.
  28. Hoang,T.T and H.P. Schweizer. 1997. Leucine biosynthesis in Pseudomonas aeruginosa: identification and characterization of leuB, encoding 3-isopropylmalate dehydrogenase. Molecular & General Genetics 254: 166-170.
  29. Hoang, T.T., Williams, S., H.P. Schweizer and Lam, J.S. 1997. Molecular genetic analysis of the region containing the essential Pseudomonas aeruginosa asd gene encoding aspartate-beta-semialdehyde dehydrogenase. Microbiology 143: 899-907.
  30. Hoang, T.T. and H.P. Schweizer. 1997. Fatty acid biosynthesis in Pseudomonas aeruginosa: cloning and characterization of the fabAB operon encoding ß-hydroxydecanoyl-acyl carrier protein dehydratase (FabA) and ß-ketoacyl-acyl carrier protein synthase I (FabB). Journal of Bacteriology 179(17): 5326-5332.
  31. Schweizer, H.P. and Hoang, T.T. 1995. An improved system for gene replacement and xylE fusion analysis in Pseudomonas aeruginosa. Gene 158: 15-22.