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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.
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Helen J. Wing, Ph.D. 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 |
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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. |
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Find out what’s new
in the “Wing lab” by visiting our Facebook page |
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For more information about studying Microbiology at
UNLV,
click the logo at the top of this page |
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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. |
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