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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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For more information about studying Microbiology at
UNLV,
click the logo at the top of this page |
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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. Accepted May 2012. 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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