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The Global Regulator DksA Reduces Transcription during T4 Infection. | LitMetric

The Global Regulator DksA Reduces Transcription during T4 Infection.

Viruses

Gene Expression and Regulation Section, Laboratory of Cell and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20814, USA.

Published: June 2018

AI Article Synopsis

  • - Bacteriophage T4 utilizes the host's RNA polymerase to transcribe different classes of promoters during infection, with varying dependencies on viral proteins and host factors.
  • - Deleting DksA or ppGpp, two transcription regulators, leads to an increase in T4 plaque size; however, ppGpp deletion does not notably change burst size or transcript levels, while DksA deletion increases burst size and early gene expression.
  • - The study suggests that DksA negatively regulates early gene transcription, which impacts T4's overall productivity during infection, indicating that its regulation of transcription may involve indirect mechanisms or other factors.

Article Abstract

Bacteriophage T4 relies on host RNA polymerase to transcribe three promoter classes: early (Pe, requires no viral factors), middle (Pm, requires early proteins MotA and AsiA), and late (Pl, requires middle proteins gp55, gp33, and gp45). Using primer extension, RNA-seq, RT-qPCR, single bursts, and a semi-automated method to document plaque size, we investigated how deletion of DksA or ppGpp, two global transcription regulators, affects T4 infection. Both ppGpp⁰ and Δ increase T4 wild type (wt) plaque size. However, ppGpp⁰ does not significantly alter burst size or latent period, and only modestly affects T4 transcript abundance, while Δ increases burst size (2-fold) without affecting latent period and increases the levels of several Pe transcripts at 5 min post-infection. In a T4 infection, Δ increases plaque size and shortens latent period, and the levels of specific middle RNAs increase due to more transcription from Pe’s that extend into these middle genes. We conclude that DksA lowers T4 early gene expression. Consequently, Δ results in a more productive wt infection and ameliorates the poor expression of middle genes in a T4 infection. As DksA does not inhibit Pe transcription in vitro, regulation may be indirect or perhaps requires additional factors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024815PMC
http://dx.doi.org/10.3390/v10060308DOI Listing

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