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Background:

 

Helen J. Wing is an Associate Professor of Molecular Microbiology in the School of Life Sciences at the University of Nevada, Las Vegas. She obtained her Ph.D. in Biochemistry from the University of Birmingham (UK) in 1997, where she studied transcriptional gene regulation in Escherichia coli.  She worked with both Prof. Stephen J.W. Busby and Prof. John R. Guest in her first post-doctoral position, where she employed biochemical approaches to study transcription.  In 2000, Helen moved to the U.S. to take a post-doctoral position with Marcia B. Goldberg M.D. at Harvard Medical School and Massachusetts General Hospital.  It was here that she became interested in the transcriptional regulation of Shigella virulence genes and antimicrobial peptides.  She joined the faculty at the University of Nevada, Las Vegas in 2005.

 

Helen J. Wing, Ph.D.

School of Life Sciences,

University of Nevada, Las Vegas

4505 S. Maryland Parkway

Las Vegas, NV 89154-4004

Office: Rm 314A

Phone: (702) 895 5382

Fax: (702) 895 3956

Email: helen.wing@unlv.edu

 

 

 

 

 

 

 

 

Biographical Sketch

Research focus:

 

The primary focus of my research laboratory is virulence gene expression in the bacterial pathogen Shigella flexneri, the causal agent of bacillary dysentery, which is estimated to kill over 1 million people each year. All four species of Shigella harbor a large virulence plasmid, which carries most of the genes required to cause disease in the human host, including those required for invasion, type III secretion and actin-based motility, a process that allows bacteria to spread from one human cell to another. We are interested in the environmental cues, the timing and the molecular events that trigger the expression of virulence genes. We are particularly interested in the complex interplay between nucleoid structuring proteins, proteins that facilitate the packaging of DNA into tiny cells, and the transcriptional regulators of virulence in Shigella VirF and VirB.

 

In a separate collaborative project we study the honey bee pathogen Paenibacillus larvae, the causal agent of American Foulbrood, which is a contributing factor in the collapse of honey bee populations globally. Notably, first and second instar larvae are susceptible to this bacterial pathogen – later instars and adult honey bees are resistant. We are exploring whether the susceptibility of the young larvae is due to a lack of protective antimicrobial peptides that are found in mature larvae and adult honey bees. We also plan to test the efficacy of the honeybee AMPs in killing P. larvae by employing MIC assays.

 

 

 

Publications

 

 

Teaching

 

 

Graduate Research

 

 

Undergraduate Research

 

 

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Selected publications:

Basta, DW, Pew KL, Immak JA, Park HS, Picker MA, Wigley AF, Hensley CT, Pearson,JS, Hartland EL and Wing HJ. 2013. Characterization of the ospZ promoter in Shigella flexneri and its regulation by VirB & H-NS. J. Bacteriol 195: 2562-2572.

Broach WH, Egan NR, Wing HJ, Payne SP and Murphy ER. 2012. VirF-independent regulation of Shigella virB transcription is mediated by the small RNA RyhB. PLoS ONE.7(6):e38592.

Africa LA, Murphy ER, Egan NR, Wigley AF, Wing HJ. 2011. The iron-responsive Fur/RyhB regulatory cascade modulates the Shigella outer membrane protease IcsP. Infect Immun. 79(11):4543-9.

Hensley CT, Kamneva OK, Levy KM, Labahn SK, Africa LA, Wing HJ. 2011. Two promoters and two translation start sites control the expression of the Shigella flexneri outer membrane protease IcsP. Arch Microbiol. 193(4):263-74.

Castellanos MI, Harrison DJ, Smith JM, Levy KM, Labahn SK and Wing HJ. 2009. VirB alleviates H-NS repression of the icsP promoter in Shigella flexneri from sites over 1 kb upstream of the transcription start site. J Bacteriol. 191: 4047-4050

Wing HJ, Goldman SR, Ally S, Goldberg MB. 2005. Modulation of an outer membrane protease contributes to the virulence defect of Shigella flexneri strains carrying a mutation in the virK locus. Inf Immun. 73:1217-1220.

Wing HJ, Yan AW, Goldman SR and Goldberg MB. 2004. Regulation of IcsP, the outer membrane protease of the Shigella actin tail assembly protein IcsA, by virulence plasmid regulators VirF and VirB. J. Bacteriol. 186: 699-705.

Wing HJ, Green J, Guest JR, Busby SJW. 2000. Role of activating region 1 of Escherichia coli FNR protein in transcription activation at class II promoters. J. Biol. Chem. 275: 29061-29065.

Li B, Wing HJ, Lee D, Wu HC, Busby SJW. 1998. Transcription activation by Escherichia coli FNR protein: similarities to, and differences from, the CRP paradigm. Nucl. Acid Res. 26: 2075-2081.

Williams SM, Savery NJ, Busby SJW, Wing HJ. 1997 Transcription activation at Class I FNR-dependent promoters: identification of the activating surface of FNR and the corresponding contact site in the C-terminal domain of the RNA polymerase alpha subunit. Nucl. Acid Res. 25: 4028-4034.

Wing HJ, Williams SM, Busby SJW. 1995. “Spacing requirements for transcription activation by Escherichia coli FNR protein.” J. Bacteriol. 177: 6704-6710.