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ESI Special Topics, September 2004
Citing URL: http://www.esi-topics.com/fmf/2004/september04-DavidSherman.html

From •>>September 2004 - [late entry]

David R. Sherman answers a few questions about this month's fast moving front in the field of Microbiology.

Field: Microbiology
Article: Regulation of the Mycobacterium tuberculosis hypoxic response gene encoding alpha-crystallin
Authors: Sherman, DR;Voskuil, M;Schnappinger, D;Liao, RL;Harrell, MI;Schoolnik, GK 
Journal: PROC NAT ACAD SCI USA, 98: (13) 7534-7539, JUN 19 2001
Addresses:
Univ Washington, Dept Pathobiol, Seattle, WA 98195 USA.
Univ Washington, Dept Pathobiol, Seattle, WA 98195 USA.
Stanford Univ, Sch Med, Div Infect Dis & Geog Med, Dept Med, Stanford, CA 94305 USA.
Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA.


ST:  Why do you think your paper is highly cited?


Tuberculosis kills about two million people each year, and TB latency contributes significantly to that dreadful situation.”

After decades of neglect, the last few years have seen a surge of interest in tuberculosis (TB) research. This paper addressed an important current issue (the nature of TB latency), and provided molecular details that are amenable to subsequent testing. Of course, it doesn't hurt that the paper provided a long list of genes expressed under particular conditions—subsequent work on any of those genes tends to cite this paper.

ST:  Does it describe a new discovery or new methodology that's useful to others?

This paper applied a very powerful and relatively new technology (transcriptome analysis by whole genome microarray) to leading hypothesis about TB latency—that a lack of oxygen drives the bacteria into a state of non-replicating persistence—for which supporting data were sketchy.

ST:  Could you summarize the significance of your paper in layman's terms?

Tuberculosis kills about two million people each year, and TB latency contributes significantly to that dreadful situation. TB latency is poorly understood, but one trigger of bacterial latency may be a lack of oxygen at certain sites in the body. This paper described a set of

bacterial genes involved in adapting to persistence under reduced oxygen conditions, and identified the bacterial regulator that drives this adaptation. As a result, we are in a much better position to understand and potentially combat TB latency.

ST:  How did you become involved in this research?

I've always been attracted to questions of how cells adapt to changing conditions. In addition, I've always tried to work on problems with a direct, tangible link to public health—even if I never do anything practical myself!End

David R. Sherman, Ph.D.
Associate Professor
Department of Pathobiology
University of Washington School of Public Health and Community Medicine
Seattle, WA, USA

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ESI Special Topics, September 2004
Citing URL: http://www.esi-topics.com/fmf/2004/september04-DavidSherman.html

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