scholarly journals Differential Expression of sigH Paralogs during Growth and under Different Stress Conditions in Mycobacterium smegmatis

2009 ◽  
Vol 191 (8) ◽  
pp. 2888-2893 ◽  
Author(s):  
Anirudh K. Singh ◽  
Bhupendra N. Singh
Keyword(s):  
Oxidative Stress ◽  
Stationary Phase ◽  
Reverse Transcriptase ◽  
Real Time ◽  
Differential Expression ◽  
Mycobacterium Smegmatis ◽  
Stress Conditions ◽  
Pcr Analysis ◽  
Stages Of Growth ◽  
And Oxidative Stress

ABSTRACT SigH regulates a transcriptional network that responds to heat and oxidative stress in mycobacteria. Seven sigH paralogs are reported to exist in the Mycobacterium smegmatis genome. A comprehensive real-time reverse transcriptase PCR analysis during different stages of growth and upon exposure to various stress conditions and antimycobacterial compounds showed differential expression of sigH paralogs during stationary phase and severalfold increases in the levels of transcription of sigH1, sigH4, sigH5, sigH6, and sigH7 under specific stress conditions.

scholarly journals The SigF Regulon in Mycobacterium smegmatis Reveals Roles in Adaptation to Stationary Phase, Heat, and Oxidative Stress

2010 ◽  
Vol 192 (10) ◽  
pp. 2491-2502 ◽  
Author(s):  
Anja Hümpel ◽  
Susanne Gebhard ◽  
Gregory M. Cook ◽  
Michael Berney
Keyword(s):  
Oxidative Stress ◽  
Stationary Phase ◽  
Sigma Factor ◽  
Mycobacterium Smegmatis ◽  
Posttranslational Regulation ◽  
Uptake System ◽  
Direct Control ◽  
Expression Change ◽  
Whole Genome Microarray ◽  
And Oxidative Stress

ABSTRACTSigF is an alternative sigma factor that is highly conserved among species of the genusMycobacterium. In this study we identified the SigF regulon inMycobacterium smegmatisusing whole-genome microarray and promoter consensus analyses. In total, 64 genes in exponential phase and 124 genes in stationary phase are SigF dependent (P< 0.01, >2-fold expression change). Our experimental data reveal the SigF-dependent promoter consensus GTTT-N(15-17)-GGGTA forM. smegmatis, and we propose 130 potential genes under direct control of SigF, of which more than 50% exhibited reduced expression in a ΔsigFstrain. We previously reported an increased susceptibility of the ΔsigFstrain to heat and oxidative stress, and our expression data indicate a molecular basis for these phenotypes. We observed SigF-dependent expression of several genes purportedly involved in oxidative stress defense, namely, a heme-containing catalase, a manganese-containing catalase, a superoxide dismutase, the starvation-induced DNA-protecting protein MsDps1, and the biosynthesis genes for the carotenoid isorenieratene. Our data suggest that SigF regulates the biosynthesis of the thermoprotectant trehalose, as well as an uptake system for osmoregulatory compounds, and this may explain the increased heat susceptibility of the ΔsigFstrain. We identified the regulatory proteins SigH3, PhoP, WhiB1, and WhiB4 as possible genes under direct control of SigF and propose four novel anti-sigma factor antagonists that could be involved in the posttranslational regulation of SigF inM. smegmatis. This study emphasizes the importance of this sigma factor for stationary-phase adaptation and stress response in mycobacteria.

scholarly journals Identification of novel small RNAs in Burkholderia cenocepacia KC-01 expressed under iron limitation and oxidative stress conditions

Microbiology ◽  
2017 ◽  
Vol 163 (12) ◽  
pp. 1924-1936 ◽  
Author(s):  
Suparna Ghosh ◽  
Chetna Dureja ◽  
Indu Khatri ◽  
Srikrishna Subramanian ◽  
Saumya Raychaudhuri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Small Rnas ◽  
Stress Conditions ◽  
Iron Limitation ◽  
Burkholderia Cenocepacia ◽  
And Oxidative Stress

scholarly journals Intra-Vitreal Administration of Microvesicles Derived from Human Adipose-Derived Multipotent Stromal Cells Improves Retinal Functionality in Dogs with Retinal Degeneration

2019 ◽  
Vol 8 (4) ◽  
pp. 510
Author(s):  
Anna Cislo-Pakuluk ◽  
Agnieszka Smieszek ◽  
Natalia Kucharczyk ◽  
Peter G.C. Bedford ◽  
Krzysztof Marycz
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Stromal Cells ◽  
Clinical Studies ◽  
Stress Conditions ◽  
In Vitro Assays ◽  
Multipotent Stromal Cells ◽  
Mitochondrial Potential ◽  
And Oxidative Stress

This study was designed to determine the influence of microvesicles (MVs) derived from multipotent stromal cells isolated from human adipose tissue (hASCs) on retinal functionality in dogs with various types of retinal degeneration. The biological properties of hASC-MVs were first determined using an in vitro model of retinal Muller-like cells (CaMLCs). The in vitro assays included analysis of hASC-MVs influence on cell viability and metabolism. Brain-derived neurotrophic factor (BDNF) expression was also determined. Evaluation of the hASC-MVs was performed under normal and oxidative stress conditions. Preliminary clinical studies were performed on ten dogs with retinal degeneration. The clinical studies included behavioral tests, fundoscopy and electroretinography before and after hASC-MVs intra-vitreal injection. The in vitro study showed that CaMLCs treated with hASC-MVs were characterized by improved viability and mitochondrial potential, both under normal and oxidative stress conditions. Additionally, hASC-MVs under oxidative stress conditions reduced the number of senescence-associated markers, correlating with the increased expression of BDNF. The preliminary clinical study showed that the intra-vitreal administration of hASC-MVs significantly improved the dogs’ general behavior and tracking ability. Furthermore, fundoscopy demonstrated that the retinal blood vessels appeared to be less attenuated, and electroretinography using HMsERG demonstrated an increase in a- and b-wave amplitude after treatment. These results shed promising light on the application of cell-free therapies in veterinary medicine for retinal degenerative disorders treatment.

scholarly journals AGEs induce caspase-mediated apoptosis of rat BMSCs via TNFα production and oxidative stress

2013 ◽  
Vol 52 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Evgeny Weinberg ◽  
Tal Maymon ◽  
Miron Weinreb
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Flow Cytometric Analysis ◽  
Annexin V ◽  
Mapk Signaling ◽  
Diabetic Rats ◽  
Protein Glycation ◽  
Pcr Analysis ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Diabetic humans and animals exhibit lower bone mass and healing, resulting from diminished bone formation. We have recently reported that type 1 diabetic rats have fewer bone marrow osteoprogenitor cells, and since the formation of advanced glycation end products (AGEs) in bone increases in diabetes, we explored possible mechanisms involved in AGE-induced apoptosis of rat bone marrow stromal cells (BMSCs). BMSCs isolated from 4-month-old rats were exposed to 10–400 μg/ml AGE–BSA for 16 h and apoptosis was quantified with PI/annexin V staining and flow cytometry. Signaling mechanisms were evaluated by preincubating the cells with appropriate inhibitors. The formation of reactive oxygen species (ROS) was quantified by flow cytometric analysis of DCFDA fluorescence and the expression of genes by RT-PCR analysis. AGE–BSA at a concentration of 400 μg/ml increased the apoptosis of BMSCs two- to threefold, an effect completely blocked by a pan-caspase inhibitor. BSA or high concentrations of glucose had no effect. AGE–BSA-induced BMSC apoptosis was attenuated by a p38 inhibitor but not by an NF-κB inhibitor. Treatment with AGE–BSA induced the expression of several pro-apoptotic ligands and receptors, most notably tumor necrosis factor α (TNFα), TRAIL, lymphotoxin alpha, CD40, and TNFR2. Furthermore, AGE–BSA-induced apoptosis was completely blocked by pirfenidone, an inhibitor of TNFα production/secretion. Finally, AGE–BSA increased the production of ROS in BMSCs, and its apoptogenic effect was blocked by the antioxidant N-acetylcysteine (N-acetyl-l-cysteine). Thus, AGE–BSA increases the apoptosis of rat BMSCs via the activation of caspases, involving TNFα production/secretion, p38 MAPK signaling, and oxidative stress. We propose that increased protein glycation, such as that occurring under hyperglycemia, causes the apoptosis of BMSCs, which might significantly contribute to the development of osteopenia in diabetic animals.

scholarly journals Stringent Response Governs the Virulence and Oxidative Stress Resistance of Francisella tularensis

2019 ◽  
Author(s):  
Zhuo Ma ◽  
Kayla King ◽  
Maha Alqahtani ◽  
Madeline Worden ◽  
Parthasarthy Muthuraman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Francisella Tularensis ◽  
Stress Resistance ◽  
Stringent Response ◽  
Oxidative Stress Response ◽  
Stress Conditions ◽  
Gram Negative ◽  
And Oxidative Stress ◽  
Starvation Conditions

AbstractFrancisella tularensis is a Gram-negative bacterium responsible for causing tularemia in the northern hemisphere. F. tularensis has long been developed as a biological weapon due to its ability to cause severe illness upon inhalation of as few as ten organisms and based on its potential to be used as a bioterror agent is now classified as a Tier 1 Category A select agent by the CDC. The stringent response facilitates bacterial survival under nutritionally challenging starvation conditions. The hallmark of stringent response is the accumulation of the effector molecules ppGpp and (p)ppGpp known as stress alarmones. The relA and spoT gene products generate alarmones in several Gram-negative bacterial pathogens. RelA is a ribosome-associated ppGpp synthetase that gets activated under amino acid starvation conditions whereas, SpoT is a bifunctional enzyme with both ppGpp synthetase and ppGpp hydrolase activities. Francisella encodes a monofunctional RelA and a bifunctional SpoT enzyme. Previous studies have demonstrated that stringent response under nutritional stresses increases expression of virulence-associated genes encoded on Francisella Pathogenicity Island. This study investigated how stringent response governs the oxidative stress response of F. tularensis. We demonstrate that RelA/SpoT-mediated ppGpp production alters global gene transcriptional profile of F. tularensis in the presence of oxidative stress. The lack of stringent response in relA/spoT gene deletion mutants of F. tularensis makes bacteria more susceptible to oxidants, attenuates survival in macrophages, and virulence in mice. Mechanistically, we provide evidence that the stringent response in Francisella contributes to oxidative stress resistance by enhancing the production of antioxidant enzymes.ImportanceThe unique intracellular life cycle of Francisella in addition to nutritional stress also exposes the bacteria to oxidative stress conditions upon its brief residence in the phagosomes, and escape into the cytosol where replication takes place. However, the contribution of the stringent response in gene regulation and management of the oxidative stress response when Francisella is experiencing oxidative stress conditions is not known. Our results provide a link between the stringent and oxidative stress responses. This study further improves our understanding of the intracellular survival mechanisms of F. tularensis.

Sign in / Sign up

Export Citation Format

Share Document