Transcriptional Regulation of Mycobacterium tuberculosis PE/PPE Genes: A Molecular Switch to Virulence

2011 ◽  
Vol 21 (3-4) ◽  
pp. 97-109 ◽  
Author(s):  
Krishnaveni Mohareer ◽  
Smanla Tundup ◽  
Seyed E. Hasnain
2020 ◽  
Vol 477 (12) ◽  
pp. 2401-2419
Author(s):  
Izaak N. Beck ◽  
Ben Usher ◽  
Hannah G. Hampton ◽  
Peter C. Fineran ◽  
Tim R. Blower

Toxin-antitoxin systems play key roles in bacterial adaptation, including protection from antibiotic assault and infection by bacteriophages. The type IV toxin-antitoxin system AbiE encodes a DUF1814 nucleotidyltransferase-like toxin, and a two-domain antitoxin. In Streptococcus agalactiae, the antitoxin AbiEi negatively autoregulates abiE expression through positively co-operative binding to inverted repeats within the promoter. The human pathogen Mycobacterium tuberculosis encodes four DUF1814 putative toxins, two of which have antitoxins homologous to AbiEi. One such M. tuberculosis antitoxin, named Rv2827c, is required for growth and whilst the structure has previously been solved, the mode of regulation is unknown. To complete the gaps in our understanding, we first solved the structure of S. agalactiae AbiEi to 1.83 Å resolution for comparison with M. tuberculosis Rv2827c. AbiEi contains an N-terminal DNA binding domain and C-terminal antitoxicity domain, with bilateral faces of opposing charge. The overall AbiEi fold is similar to Rv2827c, though smaller, and with a 65° difference in C-terminal domain orientation. We further demonstrate that, like AbiEi, Rv2827c can autoregulate toxin-antitoxin operon expression. In contrast with AbiEi, the Prv2827c promoter contains two sets of inverted repeats, which bind Rv2827c with differing affinities depending on the sequence consensus. Surprisingly, Rv2827c bound with negative co-operativity to the full Prv2827c promoter, demonstrating an unexpectedly complex form of transcriptional regulation.


2016 ◽  
Vol 475 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Soumitra Ghosh ◽  
Bhavna Padmanabhan ◽  
Adwait Anand Godbole ◽  
Priyanka Tare ◽  
Wareed Ahmed ◽  
...  

2005 ◽  
Vol 21 (10) ◽  
pp. 2563-2565 ◽  
Author(s):  
P.-E. Jacques ◽  
A. L. Gervais ◽  
M. Cantin ◽  
J.-F. Lucier ◽  
G. Dallaire ◽  
...  

2001 ◽  
Vol 183 (23) ◽  
pp. 6801-6806 ◽  
Author(s):  
Anna Milano ◽  
Francesca Forti ◽  
Claudia Sala ◽  
Giovanna Riccardi ◽  
Daniela Ghisotti

ABSTRACT The DNA region upstream of katG inMycobacterium smegmatis was cloned and sequenced. ThefurA gene, highly homologous to Mycobacterium tuberculosis furA, mapped in this region. ThefurA-katG organization appears to be conserved among several mycobacteria. The transcription pattern of furAand katG in M. smegmatisupon oxidative stress was analyzed by Northern blotting and primer extension. Although transcription of both furA andkatG was induced upon oxidative stress, transcripts covering both genes could not be identified either by Northern blotting or by reverse transcriptase PCR. Specific transcripts and 5′ ends were identified for furA and katG, respectively. By cloning M. smegmatis andM. tuberculosis DNA regions upstream of a reporter gene, we demonstrated the presence of two promoters,pfurA, located immediately upstream of thefurA gene, and pkatG, located within the terminal part of the furA coding sequence. Transcription from pfurA was induced upon oxidative stress. A 23-bp sequence overlapping the pfurA −35 region is highly conserved among mycobacteria and streptomycetes and might be involved in controlling pfurA activity. Transcription from a cloned pkatG, lacking the upstream pfurAregion, was not induced upon oxidative stress, suggesting acis-acting regulatory role of this region.


Microbiology ◽  
2002 ◽  
Vol 148 (10) ◽  
pp. 2997-3006 ◽  
Author(s):  
Marı́a P. Santangelo ◽  
Jorge Goldstein ◽  
Alicia Alito ◽  
Andrea Gioffré ◽  
Karina Caimi ◽  
...  

2010 ◽  
Vol 34 (8) ◽  
pp. S27-S27
Author(s):  
Jianqi Cui ◽  
Xiuying Pei ◽  
Qian Zhang ◽  
Bassel E. Sawaya ◽  
Xiaohong Lu ◽  
...  

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