The Mycobacterium tuberculosis mysB gene product is a functional equivalent of the Escherichia coli sigma factor, KatF

Gene ◽  
1999 ◽  
Vol 240 (2) ◽  
pp. 361-370 ◽  
Author(s):  
Nicola J. Mulder ◽  
Ros E. Powles ◽  
Harold Zappe ◽  
Lafras M. Steyn
Keyword(s):  
Escherichia Coli ◽  
Mycobacterium Tuberculosis ◽  
Gene Product ◽  
Sigma Factor ◽  
Functional Equivalent

scholarly journals Identification of Mycobacterium tuberculosis signal sequences that direct the export of a leaderless  -lactamase gene product in Escherichia coli

Microbiology ◽  
1998 ◽  
Vol 144 (6) ◽  
pp. 1619-1629 ◽  
Author(s):  
A. J. Chubb ◽  
Z. L. Woodman ◽  
F. M. P. R. da Silva Tatley ◽  
H. J. Hoffmann ◽  
R. R. Scholle ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Mycobacterium Tuberculosis ◽  
Gene Product ◽  
Signal Sequences ◽  
Lactamase Gene

scholarly journals Identification and Analysis of “Extended −10” Promoters from Mycobacteria

1998 ◽  
Vol 180 (9) ◽  
pp. 2568-2573 ◽  
Author(s):  
Murali D. Bashyam ◽  
Anil K. Tyagi
Keyword(s):  
Escherichia Coli ◽  
Mycobacterium Tuberculosis ◽  
Sigma Factor ◽  
Mycobacterium Smegmatis ◽  
Important Determinant ◽  
Comparative Assessment ◽  
Binding Domain ◽  
Site Specific ◽  
E Coli

ABSTRACT Earlier studies from our laboratory on randomly isolated transcriptional signals of mycobacteria had revealed that the −10 region of mycobacterial promoters and the corresponding binding domain in the major sigma factor are highly similar to their Escherichia coli counterparts. In contrast, the sequences in −35 regions of mycobacterial promoters and the corresponding binding domain in the major sigma factor are vastly different from their E. colicounterparts (M. D. Bashyam, D. Kaushal, S. K. Dasgupta, and A. K. Tyagi, J. Bacteriol. 178:4847–4853, 1996). We have now analyzed the role of the TGN motif present immediately upstream of the −10 region of mycobacterial promoters. Sequence analysis and site-specific mutagenesis of a Mycobacterium tuberculosispromoter and a Mycobacterium smegmatis promoter reveal that the TGN motif is an important determinant of transcriptional strength in mycobacteria. We show that mutation in the TGN motif can drastically reduce the transcriptional strength of a mycobacterial promoter. The influence of the TGN motif on transcriptional strength is also modulated by the sequences in the −35 region. Comparative assessment of these extended −10 promoters in mycobacteria and E. coli suggests that functioning of the TGN motif in promoters of these two species is similar.

A developmental gene product of Bacillus subtilis homologous to the sigma factor of Escherichia coli

Nature ◽  
1984 ◽  
Vol 312 (5992) ◽  
pp. 376-378 ◽  
Author(s):  
Patrick Stragier ◽  
Jean Bouvier ◽  
Céline Bonamy ◽  
Jekisiel Szulmajster
Keyword(s):  
Escherichia Coli ◽  
Bacillus Subtilis ◽  
Gene Product ◽  
Sigma Factor ◽  
Developmental Gene

scholarly journals Autophagy—A Story of Bacteria Interfering with the Host Cell Degradation Machinery

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 110
Author(s):  
Anna K. Riebisch ◽  
Sabrina Mühlen ◽  
Yan Yan Beer ◽  
Ingo Schmitz
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Listeria Monocytogenes ◽  
Salmonella Typhimurium ◽  
Innate Immune ◽  
Intracellular Pathogens ◽  
Response Mechanism ◽  
Pathogenic Escherichia Coli

Autophagy is a highly conserved and fundamental cellular process to maintain cellular homeostasis through recycling of defective organelles or proteins. In a response to intracellular pathogens, autophagy further acts as an innate immune response mechanism to eliminate pathogens. This review will discuss recent findings on autophagy as a reaction to intracellular pathogens, such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium tuberculosis, Staphylococcus aureus, and pathogenic Escherichia coli. Interestingly, while some of these bacteria have developed methods to use autophagy for their own benefit within the cell, others have developed fascinating mechanisms to evade recognition, to subvert the autophagic pathway, or to escape from autophagy.

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