期刊
VIRUSES-BASEL
卷 10, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/v10060308
关键词
bacteriophage T4; DksA; MotA; RNA-seq; transcriptome analysis
类别
资金
- Intramural Research Program of the NIH, National Institute of Diabetes and Digestive and Kidney Diseases
- NIH, Eunice Kennedy Shriver National Institute of Child Health and Human Development
- National Institute of General Medical Sciences of the National Institutes of Health [R43GM113546]
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 E. coli global transcription regulators, affects T4 infection. Both ppGpp(0) and Delta dksA increase T4 wild type (wt) plaque size. However, ppGpp(0) does not significantly alter burst size or latent period, and only modestly affects T4 transcript abundance, while Delta dksA increases burst size (2-fold) without affecting latent period and increases the levels of several Pe transcripts at 5 min post-infection. In a T4motA(am) infection, Delta dksA 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, Delta dksA results in a more productive wt infection and ameliorates the poor expression of middle genes in a T4motA(am) infection. As DksA does not inhibit Pe transcription in vitro, regulation may be indirect or perhaps requires additional factors.
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