Stress response of genes encoding putative stress signaling molecules of Mycobacterium tuberculosis

10.2741/2417 ◽  
2007 ◽  
Vol 12 (8-12) ◽  
pp. 4676 ◽  
Author(s):  
Subramanian Dhandayuthapani
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Stress Response ◽  
Signaling Molecules ◽  
Stress Signaling ◽  
Genes Encoding

Analysis of genetic polymorphisms affecting the four phospholipase C (plc) genes in Mycobacterium tuberculosis complex clinical isolates

Microbiology ◽  
2004 ◽  
Vol 150 (4) ◽  
pp. 967-978 ◽  
Author(s):  
C. Viana-Niero ◽  
P. E. de Haas ◽  
D. van Soolingen ◽  
S. C. Leão
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Phospholipase C ◽  
Genetic Polymorphisms ◽  
Blot Hybridization ◽  
Southern Blot Hybridization ◽  
Clinical Isolates ◽  
Significant Similarity ◽  
Genomic Deletions ◽  
Genes Encoding ◽  
Mycobacterium Africanum

The Mycobacterium tuberculosis genome contains four highly related genes which present significant similarity to Pseudomonas aeruginosa genes encoding phospholipase C enzymes. Three of these genes, plcA, plcB and plcC, are organized in tandem (locus plcABC). The fourth gene, plcD, is located in a different region. This study investigates variations in plcABC and plcD genes in clinical isolates of M. tuberculosis, Mycobacterium africanum and ‘Mycobacterium canettii’. Genetic polymorphisms were examined by PCR, Southern blot hybridization, sequence analysis and RT-PCR. Seven M. tuberculosis isolates contain insertions of IS6110 elements within plcA, plcC or plcD. In 19 of 25 M. tuberculosis isolates examined, genomic deletions were identified, resulting in loss of parts of genes or complete genes from the plcABC and/or plcD loci. Partial plcD deletion was observed in one M. africanum isolate. In each case, deletions were associated with the presence of a copy of the IS6110 element and in all occurrences IS6110 was transposed in the same orientation. A mechanism of deletion resulting from homologous recombination of two copies of IS6110 was recognized in a group of genetically related M. tuberculosis isolates. Five M. tuberculosis isolates presented major polymorphisms in the plcABC and plcD regions, along with loss of expression competence that affected all four plc genes. Phospholipase C is a well-known bacterial virulence factor. The precise role of phospholipase C in the pathogenicity of M. tuberculosis is unknown, but considering the potential importance that the plc genes may have in the virulence of the tubercle bacillus, the study of isolates cultured from patients with active tuberculosis bearing genetic variations affecting these genes may provide insights into the significance of phospholipase C enzymes for tuberculosis pathogenicity.

scholarly journals Effect of Growth State on Transcription Levels of Genes Encoding Major Secreted Antigens of Mycobacterium tuberculosis in the Mouse Lung

2004 ◽  
Vol 72 (4) ◽  
pp. 2420-2424 ◽  
Author(s):  
Lanbo Shi ◽  
Robert North ◽  
Maria Laura Gennaro
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Adaptive Immunity ◽  
Mouse Lung ◽  
Mrna Levels ◽  
Growth State ◽  
Genes Encoding ◽  
Secreted Antigens

ABSTRACT Arrest of the multiplication of Mycobacterium tuberculosis caused by expression of adaptive immunity in mouse lung was accompanied by a 10- to 20-fold decrease in levels of mRNAs encoding the secreted Ag85 complex and 38-kDa lipoprotein. esat-6 mRNA levels were high throughout infection. The data imply that multiplying and nonreplicating tubercle bacilli have different antigen compositions.

scholarly journals Whole Exome Sequencing of HIV-1 long-term non-progressors identifies rare variants in genes encoding innate immune sensors and signaling molecules

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sara Konstantin Nissen ◽  
Mette Christiansen ◽  
Marie Helleberg ◽  
Kathrine Kjær ◽  
Sofie Eg Jørgensen ◽  
...  
Keyword(s):  
Exome Sequencing ◽  
Whole Exome Sequencing ◽  
Rare Variants ◽  
Signaling Molecules ◽  
Innate Immune ◽  
Whole Exome ◽  
Genes Encoding ◽  
Hiv 1

scholarly journals Local adaptation of Mycobacterium tuberculosis on the Tibetan Plateau

2021 ◽  
Vol 118 (17) ◽  
pp. e2017831118
Author(s):  
Qingyun Liu ◽  
Haican Liu ◽  
Li Shi ◽  
Mingyu Gan ◽  
Xiuqin Zhao ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Local Adaptation ◽  
Population Genomics ◽  
Genetic Evidence ◽  
The Tibetan Plateau ◽  
Lower Altitude ◽  
Local Environments ◽  
Plausible Model ◽  
Genes Encoding

During its global dispersal, Mycobacterium tuberculosis (Mtb) has encountered varied geographic environments and host populations. Although local adaptation seems to be a plausible model for describing long-term host–pathogen interactions, genetic evidence for this model is lacking. Here, we analyzed 576 whole-genome sequences of Mtb strains sampled from different regions of high-altitude Tibet. Our results show that, after sequential introduction of a few ancestral strains, the Tibetan Mtb population diversified locally while maintaining strict separation from the Mtb populations on the lower altitude plain regions of China. The current population structure and estimated past population dynamics suggest that the modern Beijing sublineage strains, which expanded over most of China and other global regions, did not show an expansion advantage in Tibet. The mutations in the Tibetan strains showed a higher proportion of A > G/T > C transitions than strains from the plain regions, and genes encoding DNA repair enzymes showed evidence of positive selection. Moreover, the long-term Tibetan exclusive selection for truncating mutations in the thiol-oxidoreductase encoding sseA gene suggests that Mtb was subjected to local selective pressures associated with oxidative stress. Collectively, the population genomics of Mtb strains in the relatively isolated population of Tibet provides genetic evidence that Mtb has adapted to local environments.

scholarly journals Molecular detection of Multi-Drug Resistant Mycobacterium species in a Tertiary Care centre

2020 ◽  
Vol 11 (SPL2) ◽  
pp. 1-5
Author(s):  
Ancy Justin J K ◽  
Bhuvaneshwari G ◽  
Kalyani M
Keyword(s):  
Drug Resistance ◽  
Mycobacterium Tuberculosis ◽  
Target Genes ◽  
Tertiary Care ◽  
Asia Pacific ◽  
Public Health Issue ◽  
Care Hospital ◽  
Mycobacterium Species ◽  
Genes Encoding ◽  
Extra Pulmonary

Tuberculosis (TB) - one of the leading causes of adult death in the Asia-Pacific Region, is an infectious disease caused by Mycobacterium tuberculosis (MTB). TB remains a major public health issue especially in developing nations due to the lack of adequate rapid diagnostic testing facilities. Drug resistance in tuberculosis was observed nearly fifty years ago. The risk is now due to the emergence of new strains which are most resistant to the potent anti-tuberculosis drugs. The resistance to drugs in Mycobacterium tuberculosis is conferred by mutations witⱨ the genes encoding drug targets or drug converting enzymes. In suspected extra pulmonary tuberculosis cases also, fast and accurate laboratory diagnosis is of primary importance, since the techniques which are followed from past years for detecting acid-fast bacilli have many limitations. This study may also help in standardizing the technique for rapid identification of MDR TB in extra pulmonary TB patients in this Tertiary care Hospital. The current study describes the importance and use of Polymerase Chain Reaction (PCR) for the detection of Multidrug-resistant Mycobacterium species. The target genes encoding resistance to Isoniazid and Rifampicin were detected by Polymerase Cain reaction and Agarose gel electrophoresis. Among the 359 samples, 2% were resistant to botⱨ Isoniazid and Rifampicin and tⱨe prevalence of drug resistance was found to be more in adult age groups.

scholarly journals Functional interactions between Mi-2β and AP1 complexes control response and recovery from skin barrier disruption

2019 ◽  
Vol 217 (3) ◽  
Author(s):  
Sayaka Shibata ◽  
Mariko Kashiwagi ◽  
Bruce A. Morgan ◽  
Katia Georgopoulos
Keyword(s):  
Stress Response ◽  
Transcriptional Response ◽  
Selective Reduction ◽  
Skin Barrier ◽  
Human Keratinocytes ◽  
Chromatin Accessibility ◽  
Stress Signaling ◽  
Genetic Ablation ◽  
Barrier Disruption ◽  
Stress Response Genes

Keratinocytes respond to environmental signals by eliciting induction of genes that preserve skin’s integrity. Here we show that the transcriptional response to stress signaling is supported by short-lived epigenetic changes. Comparison of chromatin accessibility and transcriptional changes induced by barrier disruption or by loss of the nucleosome remodeler Mi-2β identified their striking convergence in mouse and human keratinocytes. Mi-2β directly repressed genes induced by barrier disruption by restricting AP1-enriched promoter-distal sites, occupied by Mi-2β and JUNB at steady state and by c-JUN after Mi-2β depletion or stress signaling. Barrier disruption led to a modest reduction in Mi-2β expression and a further selective reduction of Mi-2β localization at stress response genes, possibly through competition with activated c-JUN. Consistent with a repressive role at stress response genes, genetic ablation of Mi-2β did not prevent reestablishment of barrier integrity but was required for return to homeostasis. Thus, a competition between Mi-2β–repressive and activating AP1 complexes may permit rapid transcriptional response to and resolution from stress signaling.

scholarly journals Mycobacterium tuberculosis virulence-regulator PhoP interacts with alternative sigma factor SigE during acid-stress response

2017 ◽  
Vol 104 (3) ◽  
pp. 400-411 ◽  
Author(s):  
Roohi Bansal ◽  
Vijjamarri Anil Kumar ◽  
Ritesh Rajesh Sevalkar ◽  
Prabhat Ranjan Singh ◽  
Dibyendu Sarkar
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Stress Response ◽  
Sigma Factor ◽  
Acid Stress ◽  
Alternative Sigma Factor ◽  
Acid Stress Response ◽  
Virulence Regulator

scholarly journals Caenorhabditits elegans LRK-1 and PINK-1 Act Antagonistically in Stress Response and Neurite Outgrowth

2009 ◽  
Vol 284 (24) ◽  
pp. 16482-16491 ◽  
Author(s):  
Julia Sämann ◽  
Jan Hegermann ◽  
Erika von Gromoff ◽  
Stefan Eimer ◽  
Ralf Baumeister ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Parkinson Disease ◽  
Neurite Outgrowth ◽  
Physiological Role ◽  
Model Organisms ◽  
Loss Of Function ◽  
C Elegans ◽  
Genes Encoding

Mutations in two genes encoding the putative kinases LRRK2 and PINK1 have been associated with inherited variants of Parkinson disease. The physiological role of both proteins is not known at present, but studies in model organisms have linked their mutants to distinct aspects of mitochondrial dysfunction, increased vulnerability to oxidative and endoplasmic reticulum stress, and intracellular protein sorting. Here, we show that a mutation in the Caenorhabditits elegans homologue of the PTEN-induced kinase pink-1 gene resulted in reduced mitochondrial cristae length and increased paraquat sensitivity of the nematode. Moreover, the mutants also displayed defects in axonal outgrowth of a pair of canal-associated neurons. We demonstrate that in the absence of lrk-1, the C. elegans homologue of human LRRK2, all phenotypic aspects of pink-1 loss-of-function mutants were suppressed. Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background. These results provide the first evidence of an antagonistic role of PINK-1 and LRK-1. Due to the similarity of the C. elegans proteins to human LRRK2 and PINK1, we suggest a common role of both factors in cellular functions including stress response and regulation of neurite outgrowth. This study might help to link pink-1/PINK1 and lrk-1/LRRK2 function to the pathological processes resulting from Parkinson disease-related mutants in both genes, the first manifestations of which are cytoskeletal defects in affected neurons.

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