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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

ABSTRACT: BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

PROVIDER: PRJNA695525 | ENA |

REPOSITORIES: ENA

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BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

Project description:The cystic fibrosis transmembrane conductance regulator (CFTR) gene lies within a TAD in which multiple cis-regulatory elements (CREs) and transcription factors (TFs) regulate its cell-specific expression. The CREs are recruited to the gene promoter by a looping mechanism that depends upon both architectural proteins and specific TFs. An siRNA screen to identify TFs coordinating CFTR expression in airway epithelial cells suggested an activating role for BTB Domain and CNC Homolog 1 (BACH1). BACH1 is a ubiquitous master regulator of the cellular response to oxidative stress. Here we show that BACH1 may have a dual effect on CFTR expression by direct occupancy of CREs at physiological oxygen (~8%), while indirectly modulating expression under conditions of oxidative stress. Hence BACH1, can activate or repress the same gene, to fine tune expression in response to environmental cues such as cell stress. Furthermore, our 4C-seq data suggest that BACH1 can also directly regulate CFTR gene expression by modulating locus architecture through occupancy at known enhancers and structural elements, and depletion of BACH1 alters the higher order chromatin structure.

2021-11-17 | GSE165718 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

2021-11-17 | GSE165717 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

2021-11-17 | GSE165716 | GEO

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [4C-seq]

| PRJNA695528 | ENA

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [ChIP-seq]

| PRJNA695529 | ENA

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

Project description:BACH1, the master regulator of oxidative stress, modulates CFTR gene expression [RNA-seq]

| PRJNA695530 | ENA

BACH1, the master regulator of oxidative stress, modulates CFTR gene expression

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-17 | GSE165719 | GEO

BACH1, the master regulator of oxidative stress, has a dual effect on CFTR expression.

Project description: Not available

| S-EPMC8589331 | biostudies-literature

Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Aflatoxin B1 (AFB1) is amongst the mycotoxins commonly affecting human and animal health, raising global food safety and control concerns. The mechanisms underlying AFB1 toxicity are poorly understood. Moreover, antidotes against AFB1 are lacking. Genome-wide CRISPR/Cas9 knockout screening in porcine kidney cells identified the transcription factor BTB and CNC homolog 1 (BACH1) as a gene required for AFB1 toxicity. The inhibition of BACH1 expression in porcine kidney cells and human hepatoma cells resulted in increased resistance to AFB1. BACH1 depletion attenuates AFB1-induced oxidative damage via the upregulation of antioxidant genes.

2022-03-25 | GSE199384 | GEO

BACH1 is a central regulator of glutathione metabolism, cellular necrosis and host resistance in Mycobacterium tuberculosis infection

Project description:Background. An exacerbated oxidative stress response can regulate cellular necrosis by triggering lipid peroxidation in an iron-dependent manner and this form of necrotic death has been implicated in Mycobacterium tuberculosis (Mtb) pathogenesis. Here we examined the role of Bach1, a transcription factor that represses a major set of antioxidant genes, in regulating host resistance to Mtb. We found that BACH1 expression is associated with and predicts active pulmonary tuberculosis in humans. In response to Mtb infection in vitro and in vivo, ablation of Bach1 increased the levels of glutathione as well as enhanced the expression of Gpx4, an enzyme that regulates lipid peroxidation. Consistent with these observations, Bach1-/- macrophages exhibited increased resistance to Mtb-induced cell death and infected Bach1-deficient mice displayed a striking reduction in bacterial loads as well as pulmonary necrosis and lipid peroxidation accompanied by enhanced survival. In addition, single-cell RNAseq analysis of the lungs of Mtb-infected Bach1-/- mice revealed an enrichment of genes associated with suppression of ferroptosis. Finally, deletion of Bach1 in B6.Sst1S mice, an inbred strain that exhibits the necrotic lung pathology similar to that seen in human TB, enhanced host resistance to Mtb while significantly reducing tissue necrosis. These findings identify Bach1 and its regulation of the oxidative stress response as an important modulator of cellular and tissue necrosis as well as host resistance in Mtb infection.

2023-09-07 | GSE236853 | GEO

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