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Scientific Overview Research Interest Summary Principal Investigators    Yuri Bushkin, Ph.D.
   Theresa Chang, Ph.D.
   Neeraj Chauhan, Ph.D.
   Véronique Dartois, Ph.D.
   Loren Day, Ph.D.
   Karl Drlica, Ph.D.
   David Dubnau, Ph.D.
   Eliseo A. Eugenin, Ph.D.
   Marila Gennaro, M.D.
   Gilla Kaplan, Ph.D.
   Fred Kramer, Ph.D.
   Barry Kreiswirth, Ph.D.
   Leonard Mindich, Ph.D.
   Arkady Mustaev, Ph.D.
   Harvey Penefsky, Ph.D.
   David Perlin, Ph.D.
   Richard Pine, Ph.D.
   Abraham Pinter, Ph.D.
   Marcela Rodriguez, Ph.D.
   Issar Smith, Ph.D.
   Alicia Solórzano, Ph.D.
   Patricia Soteropoulos, Ph.D.
   Sanjay Tyagi, Ph.D.
   Chaoyang Xue, Ph.D.
   Xilin Zhao, Ph.D.

   Research Faculty
   Eugenie Dubnau, Ph.D.
   Jeanette Hahn, Ph.D.
   Salvatore Marras, Ph.D.
   Lisa K. Ryan, Ph.D.
   Lanbo Shi, Ph.D.

Junior Faculty Members
 
Issar Smith, Ph.D.
 



Recent Articles

Manganelli R, Voskuil MI, Schoolnik GK, Smith I
The Mycobacterium tuberculosis ECF sigma factor sigmaE: role in global geneexpression and survival in macrophages.
Mol Microbiol 2001 Jul;41(2):423-37
PMID: 11489128

In previously published work, we identified three Mycobacterium tuberculosis
sigma (sigma) factor genes responding to heat shock (sigB, sigE and sigH). Two
of them (sigB and sigE) also responded to SDS exposure. As these responses to
stress suggested that the sigma factors encoded by these genes could be involved
in pathogenicity, we are studying their role in physiology and virulence. In
this work, we characterize a sigE mutant of M. tuberculosis H37Rv. The sigE
mutant strain was more sensitive than the wild-type strain to heat shock, SDS
and various oxidative stresses. It was also defective in the ability to grow
inside both human and murine unactivated macrophages and was more sensitive than
the wild-type strain to the killing activity of activated murine macrophages.
Using microarray technology and quantitative reverse transcription-polymerase
chain reaction (RT-PCR), we started to define the sigmaE regulon of M.
tuberculosis and its involvement in the global regulation of the stress induced
by SDS. We showed the requirement for a functional sigE gene for full expression
of sigB and for its induction after SDS exposure but not after heat shock. We
also identified several genes that are no longer induced when sigmaE is absent.
These genes encode proteins belonging to different classes including
transcriptional regulators, enzymes involved in fatty acid degradation and
classical heat shock proteins.


   
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