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Identification of a transcription factor, PunR, that regulates the purine and purine nucleoside transporter punC in E. coli

ABSTRACT: Identification of a transcription factor, PunR, that regulates the purine and purine nucleoside transporter punC in E. coli

PROVIDER: PRJNA701011 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13668410.fastq.gz	Fastqsanger.gz
	SRR13668411.fastq.gz	Fastqsanger.gz

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Identification of a transcription factor, PunR, that regulates the purine and purine nucleoside transporter punC in E. coli

Project description:Many genes in bacterial genomes are of unknown function, often referred to as y-genes. Recently, the analytic methods have divided bacterial transcriptomes into independently modulated sets of genes (iModulons). Functionally annotated iModulons that contain y-genes lead to testable hypotheses to elucidate y-gene function. The inversely correlated expression of a putative transporter gene, ydhC, relative to purine biosynthetic genes, has led to the hypothesis that it encodes a purine-related transporter and revealed a LysR-family regulator, YdhB, with a predicted 23-bp palindromic binding motif. RNA-Seq analysis of a ydhB knockout mutant confirmed the YdhB-dependent activation of ydhC in the presence of adenosine. The deletion of either the ydhC or the ydhB gene led to a substantially decreased growth rate for E. coli in minimal medium with adenosine, inosine, or guanosine as the nitrogen source. Taken together, we provide clear evidence that YdhB activates the expression of the ydhC gene that encodes a purine transporter in E. coli. We propose that the genes ydhB and ydhC be re-named as punR and punC, respectively.

2021-07-16 | GSE166465 | GEO

A novel transcription factor PunR and Nac are involved in purine and purine nucleoside transporter punC regulation in E. coli

Project description:Recently, novel analytic methods have divided bacterial transcriptomes into independently modulated sets of genes (iModulons). Functionally annotated iModulons that contain y-genes lead to testable hypotheses to elucidate y-gene function. The inversely correlated expression of a putative transporter gene, ydhC, relative to purine biosynthetic genes, has led to the hypothesis that it encodes a purine-related transporter and revealed a LysR-family regulator, YdhB, with a predicted 23-bp palindromic binding motif. RNA-Seq analysis of a ydhB knockout mutant confirmed the YdhB-dependent activation of ydhC in the presence of adenosine. The deletion of either the ydhC or the ydhB gene led to a substantially decreased growth rate for E. coli in minimal medium with adenosine, inosine, or guanosine as the nitrogen source. Taken together, we provide clear evidence that YdhB activates the expression of the ydhC gene that encodes a novel purine transporter in E. coli. We propose that the genes ydhB and ydhC be re-named as punR and punC, respectively.

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A novel transcription factor PunR and Nac are involved in purine and purine nucleoside transporter punC regulation in E. coli

Project description:A novel transcription factor PunR and Nac are involved in purine and purine nucleoside transporter punC regulation in E. coli

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Identification of a transcription factor, PunR, that regulates the purine and purine nucleoside transporter punC in E. coli.

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Project description:An increasing body of evidence emphasizes the role of metabolic reprogramming in immune cells to fight off infections. However, little is known about the regulation of metabolite transporters that facilitate and support metabolic demands. In this study, we found that the expression of Equilibrative Nucleoside Transporter 3 (ENT3, encoded by SoLute Carrier family 29 member 3, Slc29a3) is part of the innate immune response which is rapidly upregulated upon pathogen insults. The transcription of Slc29a3 is directly under the regulation of IFN-induced signaling, positioning this metabolite transporter as an Interferon-stimulated gene (ISG). Suprisingly, we unveil that several viruses, including SARS-CoV2, require ENT3 to facilitate their entry into the cytoplasm. The removal or suppression of ENT3 expression is sufficient to significantly decrease viral replication in vitro and in vivo. Our study reveals that ENT3 is a pro-viral ISG co-opted by some viruses for a survival advantage.

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