Old Dominion University
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College of Sciences


Department of Biological Sciences




Dr. Dayle A. Daines

Assistant Professor of Biological Sciences

Education:

Postdoctoral Fellow, 1999-2002
University of Missouri-Columbia School of Medicine, Columbia, MO

Ph.D. 1999, Microbiology & Immunology
University of Rochester School of Medicine & Dentistry, Rochester, NY

M.S. 1998, Microbiology & Immunology
University of Rochester School of Medicine & Dentistry, Rochester, NY

B.Sc. 1995, Cellular, Molecular, and Microbial Biology
University of Calgary, Calgary, Alberta, Canada

Employment:

Mercer University School of Medicine, 2008-2012
University of California, Davis School of Medicine, 2005-2008
Lawrence Livermore National Laboratory, 2004-2005
Seattle Biomedical Research Institute, 2002-2004

Teaching Responsibilities:

Biol 430/530 - Microbial Pathogenesis

Research Interests:

The current focus of my lab is on how otitic pathogens can survive antibiotic therapy and the immune response to cause recurrent disease. In particular, we study the mechanisms used by the human-adapted Gram-negative bacterium, unencapsulated (nontypeable) Haemophilus influenzae, to cause otitis media. Our overall hypothesis is that the organism’s ability to survive and cause recurrent infection is facilitated by gene pairs known as toxin-antitoxin (TA) modules. These operons are highly conserved across many Proteobacteria and are also found in the Archaea. We are interested in the type II TA loci, those that code for protein antitoxins which bind to their cognate toxins during periods of normal growth. When bound in a complex, the TA protein pair is nontoxic. However, under conditions of stress, the more labile antitoxin can be degraded by induced intracellular proteases, freeing the more stable toxin to exert its effects. Many of the characterized toxins are ribonucleases that target the mRNA pool in the microorganism, arresting growth and resulting in a reversible bacteriostatic state. This is beneficial because it allows the bacterium to become tolerant to antimicrobials, as most target essential cellular functions necessary for growth and division. Once the stress is lifted, the organism can recover from this dormant state and start growing normally again. To investigate this, we are using a combination of genetic, biochemical, and molecular approaches. This project is funded by the National Institute on Deafness and Other Communication Disorders, National Institutes of Health.

Selected Publications:

Cline, S.D., S. Saleem and D.A. Daines. Regulation of the vapBC-1 toxin-antitoxin locus of nontypeable Haemophilus influenzae. PLoS One. 2012;7(3):e32199.

Ren, D., K.N. Nelson, P.N. Uchakin, A.L. Smith, X.X. Gu and D.A. Daines. Characterization of extended co-culture of nontypeable Haemophilus influenzae with primary human respiratory tissues. Exp Biol Med (Maywood). 2012 May 1;237(5):540-7.

Ren, D. and D.A. Daines. Use of the EpiAirway model to characterize long-term host-pathogen interactions. J Vis Exp. 2011 Sep 2;(55):e3261. doi: 10.3791/3261.

Guo M., D. Daines, J. Tang, Q. Shen, R.M. Perrin, Y. Takada, S.Y. Yuan and M.H. Wu. 2009. Fibrinogen-gamma C-terminal fragments induce endothelial barrier dysfunction and microvascular leak via integrin-mediated and RhoA-dependent mechanism. Arterioscler Thromb Vasc Biol. 29(3):394-400.

Daines D.A., M.H. Wu and S.Y. Yuan. 2007. VapC-1 of nontypeable Haemophilus influenzae is a ribonuclease. J Bacteriol. 189:5041-8.

Reynoso R., R.M. Perrin, J.W. Breslin, D.A. Daines, K.D. Watson, D.M. Watterson, M.H. Wu and S. Yuan. 2007. A role for long chain myosin light chain kinase (MLCK-210) in microvascular hyperpermeability during severe burns. Shock. 2007 Nov;28(5):589-95.

Daines, D.A., M. Bothwell, J. Furrer, W. Unrath, K. Nelson, J. Jarisch, N. Melrose, L. Greiner, M. Apicella, and A.L. Smith. 2005. Haemophilus influenzae luxS mutants form a biofilm and exhibit increased virulence. Microb Pathog. 39:87-96.

Daines, D.A., J. Jarisch and A.L. Smith. 2004. Identification and characterization of a nontypeable Haemophilus influenzae putative toxin-antitoxin locus. BMC Microbiol. 4:30.

Daines, D.A. and A.L. Smith. 2004. Construction of a nontypeable Haemophilus influenzae-specific ectopic delivery vector. J Microbiol Methods 57:421-424.

Vann, W.F., D.A. Daines, A.S. Murkin, M.E. Tanner, D.O. Chaffin, C.E. Rubens, J. Vionnet, P. Guerry and R.P. Silver. 2004. The NeuC protein of Escherichia coli K1 is a uridine diphosphate N-acetylglucosamine 2-epimerase. J Bacteriol. 186:706-712.

Coleman, H.N., D.A. Daines, J. Jarisch and A.L. Smith. 2003. Chemically defined media for growth of Haemophilus influenzae strains. J Clin Microbiol. 41:4408-4410.

Daines, D.A., L.A. Cohn, H.N. Coleman, K.S. Kim, and A.L. Smith. 2003. Haemophilus influenzae Rd KW20 has virulence properties. J Med Microbiol. 52:277-282.

Daines, D.A., M. Granger-Schnarr, M. Dimitrova, and R.P. Silver. 2002. Use of a LexA-based system to identify protein:protein interactions in vivo. Methods Enzymol. 358:153-161.

Daines, D.A. and A.L. Smith. 2001. Design and construction of a Haemophilus influenzae conjugal expression system. Gene 281: 95-102.

Daines, D.A. and R.P. Silver. 2000. Evidence for multimerization of Neu proteins involved in polysialic acid synthesis in Escherichia coli K1 using improved LexA-based vectors. J Bacteriol. 182:5267-5270.

Daines, D.A., L.F. Wright, D.O. Chaffin, C.E. Rubens, and R.P. Silver. 2000. NeuD plays a role in the synthesis of sialic acid in Escherichia coli K1. FEMS Microbiol Lett. 189:281-284.

Mattatall, N.R., D.A. Daines, S.-L. Liu, and K.E. Sanderson. 1996. Salmonella typhi contains identical intervening sequences in all seven rrl genes. J Bacteriol. 178:5323-5326.

Contact Information:

Department of Biological Sciences
Old Dominion University
Phone: 757-683-3604
Email: ddaines@odu.edu