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Mycobacterium tuberculosis m4C DNA methyltransferase Rv3204 promotes mycobacteria survival under oxidative stress

ABSTRACT: Mycobacterium tuberculosis m4C DNA methyltransferase Rv3204 promotes mycobacteria survival under oxidative stress

PROVIDER: PRJNA586773 | ENA |

REPOSITORIES: ENA

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Mycobacterium tuberculosis m4C DNA methyltransferase Rv3204 promotes mycobacteria survival under oxidative stress

Project description:ROS can damage cellular components and is a key player in many cellular signaling. Tuberculosis remains a major global public health concern largely due to the ability of its causative agent-Mycobacterium tuberculosis (Mtb) to subvert ROS toxicity. DNA methylation deficiency was previously shown to attenuate the Mtb virulence. But the role of DNA methyltransferase in Mycobacteria survival and the link with ROS are unknown. Mycobacterial protein Rv3204 is a DNA methyltransferase specific for N4-methylcytosine instead of N6-methyladenine (m6A) or 5-methylocytosine (m5C). The survival rate of m4C methyltransferase deletion mutants was lowered, accompanied by higher accumulation of ROS and failure of upregulating the transcription of gene engaged in ROS clearance upon rifampin(Rif) exposure.

2019-11-01 | GSE139646 | GEO

Experimental selection of long-term intracellular mycobacteria

Project description:Some intracellular bacteria are known to cause long-term infections for periods of time that last decades without compromising the viability of the host. Although of critical importance, the changes that intracellular bacteria suffer during this long process of residence in a host cell environment remain obscure. Here, we report an experimental approach to study the adaptations of intracellular mycobacteria forced by a long-term intracellular lifestyle. Long-term infection of host macrophages with mycobacteria was maintained for a period of years. Mycobacteria in the long-term infected macrophages underwent an adaptation process leading to impaired phenolic glycolipids (PGL) synthesis, preference for glucose as a carbon source and neutral lipids accumulation. These changes correlated with increased survival of mycobacteria in macrophages and mice during re-infection and specific expression of stress- and survival-related genes. Our findings identify bacterial traits implicated in the establishment of long-term cellular infections and represent a tool for understanding the physiological states of bacteria living in fluctuating intracellular environments.

2014-12-31 | GSE49976 | GEO

Effect of Pro- and anti-inflammatory lipids in intracellular survival and killing of mycobacteria

Project description:Mouse macrophages J774A.1 were pre-treated with the anti-inflammatory lipid eicosapenaenoic acid (EPA) or the pro-inflammatory lipid ceramide (Cer) for 3h. Macrophages were then infected with Mycobacterium smegmatis for 1h, and total RNA was collected. In a parallel experiment, infected macrophages were infected for 1h, 4h and 24h. At these time points, macrophages were lysed, bacteria was collected and quantified by the Colony Forming Units (CFU) Assay. This provided the kinetics of the killing of Mycobacteria inside mouse macrophages. CFU experiments revealed that cells pre-treated with EPA showed an increased number of bacteria inside macrophages, in contrast to cells pre-treated with Cer. To dissect the molecular mechanisms involved in the survival and killing of mycobacteria infected macrophages, mediated by lipids, gene expression studies were performed.

2015-01-20 | GSE27277 | GEO

Nontuberculous mycobacteria

Project description:Nontuberculous mycobacteria Metagenome

| PRJNA779755 | ENA

Activating Parkin-dependent mitophagy alleviates oxidative stress, apoptosis, and promotes random-pattern skin flaps survival

Project description:The random-pattern skin flap is a crucial technique in reconstructive surgery and flap necrosis caused by ischemia/reperfusion injury is a major postoperative complication. Herein, we investigated the mechanism of mitophagy induced by Melatonin (ML) and its effect on the survival of skin flaps. Our results demonstrated that ML could activate mitophagy, ameliorate oxidative stress and alleviate apoptosis in TBHP-stimulated human umbilical vein endothelial cells in vitro. Inhibiting ML-induced mitophagy considerably abolished its protective effects. Moreover, knockdown of Parkin by siRNA inhibited ML-induced mitophagy, and subsequently exacerbated oxidative stress and apoptosis. Further study demonstrated that inhibition of AMPK reversed these protective effects of ML and downregulated the expression of TFEB. In the vivo study, ML effectively promoted flap survival by activating mitophagy and subsequently ameliorating oxidative stress and mitigating apoptosis. These results established that ML is a potent agent capable for increasing random-pattern skin flap survival by activating Parkin-dependent mitophagy through the AMPK-TFEB signaling pathway.

2022-06-29 | GSE203609 | GEO

AMPK promotes survival of c-Myc positive melanoma cells by suppressing oxidative stress

Project description:AMPK promotes survival of c-Myc positive melanoma cells by suppressing oxidative stress

| PRJNA427304 | ENA

Mycobacteria species

Project description:Mycobacteria species Raw sequence reads

| PRJNA401515 | ENA

Mycobacteria

Project description:Complete genome sequence of environmental Mycobacteria isolated from water

| PRJNA767558 | ENA

RNA Methyltransferase METTL14 Promotes Breast Cancer Growth and Progression

Project description:We investigated the role of RNA N6-adenosine methyltransferase protein METTL14 that supports breast cancer growth and progression, and we showed METTL14 knockdown inhibited long-term survival, migration as well as invasion of breast cancer cells.

2018-12-26 | GSE81164 | GEO

Activating Parkin-dependent mitophagy alleviates oxidative stress, apoptosis, and promotes random-pattern skin flaps survival

Project description:Activating Parkin-dependent mitophagy alleviates oxidative stress, apoptosis, and promotes random-pattern skin flaps survival

| PRJNA841583 | ENA