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Defining the interplay of carbon dioxide and the carbonic anhydrase CanB in regulating Mycobacterium tuberculosis PhoPR signaling and virulence

ABSTRACT: Defining the interplay of carbon dioxide and the carbonic anhydrase CanB in regulating Mycobacterium tuberculosis PhoPR signaling and virulence

PROVIDER: PRJNA823015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18594928.fastq.gz	Fastqsanger.gz
	SRR18594929.fastq.gz	Fastqsanger.gz
	SRR18594930.fastq.gz	Fastqsanger.gz
	SRR18594931.fastq.gz	Fastqsanger.gz
	SRR18594932.fastq.gz	Fastqsanger.gz

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Global transcriptomic changes following elevated carbon dioxide (5%) in the wild-type (WT) and mutant (M2; RNAi-knockdown line of carbonic anhydrase (CA2)) Nannochloropsis oceanica IMET1: Illumina sequencing

Project description:In Nannochloropsis oceanica IMET1, transcript knockdown of a cytosolic carbonic anhydrase (CA2; g2018) specifically inhibited by HC resulted in ~45%, ~30% and ~40% elevation of photosynthetic oxygen evolution rate, growth rate and biomass accumulation rate under high CO2 (5% ), respectively. This CA2-knockdown mutant is demonated as M2. To probe mechanistic links underlying the mutant (M2; RNAi-knockdown line of carbonic anhydrase (CA2)) phenotypes, temporal transcriptomic profiles are compared between RNAi-knockdown line of carbonic anhydrase (CA2) and WT, at 12 h and 24h under high CO2 (5%).

2020-10-28 | GSE115445 | GEO

Defining the interplay of carbon dioxide and the carbonic anhydrase CanB in regulating Mycobacterium tuberculosis PhoPR signaling and virulence

Project description:Regulation of M. tuberculosis gene expression by carbon dioxide at acidic and neutral pH.

2025-02-04 | GSE200125 | GEO

carbonic anhydrase (1 or 2) simple or double mutants-Comparative transcriptome analysis between carbonic anhydrase mutants and wild type Arabidopsis

Project description:cea05-01_carbonic-anhydrase - carbonic anhydrase (1 or 2) simple or double mutants - Identification of genes differentially expressed in leaves of single CA1 and CA2 T-DNA insertional mutants and in the corresponding double mutant vs wild type - CA1 (At3g01500) and CA2 (At5g14740) T-DNA insertional mutant lines, the double (CA1+CA2) mutant and wild type Arabidopsis seeds were sown in soil in a phytotron. Leaves were harvested 40 days later for RNA extraction

2012-03-25 | GSE36625 | GEO

carbonic anhydrase (1 or 2) simple or double mutants-Comparative transcriptome analysis between carbonic anhydrase mutants and wild type Arabidopsis

2012-03-25 | E-GEOD-36625 | biostudies-arrayexpress

RNA-Seq analysis of Oryza sativa, ssp. japonica, cv. Kitaake leaves from plants lacking carbonic anhydrase in the chloroplast

Project description:The aim of this experiment was to assess the impact on the transcriptome of relocalisaiton of carbonic anhydrase activity from the chloroplast to the cytosol in Oryza sativa, ssp. japonica, cv. Kitaake. Four genome edited lines and one wil-type control line were analysed.

2024-06-10 | E-MTAB-14111 | biostudies-arrayexpress

Carbonic Anhydrase 2 is Required for Maintaining Metabolic Homeostasis of Human Articular Chondrocytes

Project description:Carbonic Anhydrase 2 is Required for Maintaining Metabolic Homeostasis of Human Articular Chondrocytes

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Carbonic anhydrase 13 decreases bone metastasis of iCSCL-10A breast cancer stem cells

Project description:Carbonic anhydrase 13 decreases bone metastasis of iCSCL-10A breast cancer stem cells

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The carbonic anhydrase inhibitor ethoxzolamide inhibits the Mycobacterium tuberculosis PhoPR regulon and Esx-1 secretion and attenuates virulence

Project description:The purpose of this study was to examine how ethoxzolamide modulates gene M. tuberculosis gene expression at acidic pH. We observed that ethoxzolamide downregulates genes of the PhoPR regulon.

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Carbonic Anhydrase 2 is Required for Maintaining Metabolic Homeostasis of Human Articular Chondrocytes

Project description:Objective: To examine the role of carbonic anhydrase II (CA2 gene), the most efficient isoform in the CA family of zinc-containing metalloenzymes, in chondrocyte metabolism. Methods: CA2 expression was measured in human and mouse osteoarthritic cartilage. RNA-seq was performed in C28/I2 cells in which CA2 was silenced. Normal human chondrocytes were cultured under normoxia (21% oxygen) or hypoxia (2% oxygen) following CA2 knockdown. Cell metabolism was studied by measuring extracellular lactate production, glucose consumption, intracellular ADP/ATP, intracellular pH, and ROS production. Glycolysis was measured using Seahorse XF96 analyzer. The effect of CA2 knockdown on anabolic and catabolic markers was measured following treatment with IL-1. Effects of CA2 was examined on cell proliferation, cell-cycle distribution, colony-formation, and migration. Results: CA2 was highly elevated in human and murine osteoarthritic cartilage. RNA-seq analysis revealed that processes related to glycolysis, apoptosis and TNF signaling were perturbed in cells lacking CA2. CA2 expression was 10-fold higher under hypoxia and its knockdown caused decreased extracellular lactate production, increased ADP/ATP ratio, impaired glycolysis, decreased glycolytic capacity and lowered the expression of glycolysis rate-limiting enzymes, but did not affect intracellular pH and ROS production. CA2 deficiency disturbed chondrocyte anabolic and catabolic equilibrium. CA2 knockdown suppressed chondrocyte migration and proliferation and induced cell-cycle arrest. Conclusion: This study unravels a novel role of CA2 in chondrocyte metabolism and inflammation. These findings indicate that CA2 is required for the maintenance of chondrocyte metabolic homeostasis. Future work is needed to further illuminate the mechanistic and functional role of CA2 in osteoarthritis development.

2022-03-17 | GSE184062 | GEO

Carbonic anhydrase 2 facilitates sorafenib resistance by counteracting MCT4-mediated intracellular pH dysregulation in hepatocellular carcinoma

Project description:Sorafenib, the first targeted therapy for hepatocellular carcinoma (HCC), has been utilized in clinics over a decade. However, its effectiveness is severely hindered by the acquired drug resistance, the mechanisms of which remain largely elusive. In this study, we identify that carbonic anhydrase 2 (CA2) is a key regulator of sorafenib resistance. Mechanistically, sorafenib treatment decreases intracellular pH (pHi) by suppressing monocarboxylate transporter 4 (MCT4) expression, while high levels of CA2 counteract MCT4-mediated pHi dysregulation upon sorafenib treatment, maintaining pHi homeostasis to facilitate cell survival and sorafenib resistance. Targeting CA2 re-sensitizes resistant HCC cells to sorafenib both in vitro and in vivo. Importantly, analysis of clinical samples demonstrates a strong correlation between CA2 expression levels and the therapeutic efficacy of sorafenib in HCC patients. Our findings highlight the significance of CA2 in facilitating sorafenib resistance and propose targeting CA2 as a potential strategy for overcoming sorafenib resistance in HCC patients.

2024-10-24 | PXD056884 | Pride

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