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A phage-encoded host transcription modulator, Htm, reprograms the transcriptome of ESBL Escherichia coli

During phage infection, phages reprogram their host to secure energy, building blocks for their genome, and proteins, as well as the transcription and translation machinery required to replicate their genome and produce phage particles. This also includes reprogramming the host transcriptome to modify host gene expression and align it with the needs of the phage during infection. In this study,…

A bacterial virus, known as a phage, manipulates its host Escherichia coli to alter its genetic expression in order to gather necessary resources for its own replication and particle production. Scientists have identified a protein, Htm, encoded by the phage Mosigvirus AV110, which significantly impacts the gene expression of antibiotic-resistant E. coli.

When overexpressed, Htm slows the growth of ESBL-E. coli and causes condensation of its DNA. The protein is structurally comparable to bacterial enhancer-binding proteins, and it binds single-stranded DNA, thereby regulating the expression of over 700 E. coli genes upon introduction. Most of these genes were upregulated, which are involved in various pathways, including galactose metabolism and pentose and glucuronate interconversions.

These processes may facilitate the synthesis of crucial components like purines, pyrimidines, and histidine, which are essential for phage genome replication, transcription, and translation. Additionally, Htm increases energy production by upregulating acetyl-CoA availability, primarily due to enhanced fatty acid degradation. Concurrently, it decreases the expression of genes involved in flagellar assembly and multiple two-component systems.

Ultimately, Htm enhances phage progeny production by boosting nucleotide, amino acid, and energy availability, while suppressing non-essential processes, such as flagella formation.

Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

Read the original at biorxiv.org →

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