![]() We explicitly show that adaptation to loss of CRP frequently occurs via mutations in the ptsG promoter. To address how Escherichia coli can cope up with such a system-wide upset, we adaptively evolved Δcrp mutant in the presence of glucose. Additionally, we quantitatively demonstrate that the loss of CRP unbalances proteome allocation, favouring stress or hedging related functions over growth-enhancing functions. Here, we reveal that the deletion of CRP results in metabolic dysregulation with significant perturbation in protein biosynthesis machinery coupled to impaired glucose import. However, in presence of glucose, coordination of global transcriptional regulator cAMP-CRP with such physiological resources, remain elusive. ribosomes, RNA polymerase, metabolites and cofactors) and transcription factors that work together for optimal growth. These results provide an apparent example of transcription factor cross-talk, which can have significant consequences for the host, and may represent a constraint on lateral gene transfer.īacterial gene expression is governed by two synergistic mechanisms: growth-rate dependent global machinery (e.g. The rac locus ydaST genes, when derepressed, exerted a toxicity indicated by cell filamentation through an unknown mechanism. Our transcriptome analysis supported by in vivo and in vitro assays showed that C protein directly silenced the expression of the RacR repressor to affect the Rac prophage-related genes. Surprisingly, we found that the cell morphology defect was solely dependent on the C regulator. ![]() Our study characterized the unexpected phenotype of Escherichia coli cells, which manifested as extensive cell filamentation triggered by acquiring the Csp231I R-M system from Citrobacter sp. In some R-M systems, the host also accepts a cis-acting transcription factor (C protein), which regulates the counteracting activities of REase and MTase to avoid host self-restriction. To protect the host cell's DNA, there is also a methyltransferase (MTase), which prevents DNA cleavage by the cognate REase. In acquiring a Type II R-M system via horizontal gene transfer, the new hosts become more resistant to phage infection, through the action of a restriction endonuclease (REase), which recognizes and cleaves specific target DNAs. Restriction-modification (R-M) systems represent an effective mechanism of defence against invading bacteriophages, and are widely spread among bacteria and archaea. Unlike type II toxin-antitoxin systems in which transcriptional regulation involves complexes of the toxin and antitoxin, repression by RacR is sufficient to keep ydaS transcriptionally silent. Here, using genetics, biochemistry, and bioinformatics, we show that its essentiality derives from its role as a transcriptional repressor of the ydaS and ydaT genes, whose products are toxic to the cell. coli, we realized that the protein RacR, a putative transcription factor encoded by a gene on the rac prophage, is an essential protein. ![]() While studying transcription factors encoded in horizontally acquired regions in E. coli are rarely essential, and when they are essential, they are largely toxin-antitoxin systems. IMPORTANCE Transcription factors in the bacterium E. coli K-12 is attributed to its role in transcriptionally repressing toxin gene(s) called ydaS and ydaT, which are adjacent to and coded divergently to racR. We have shown that the essentiality of racR in E. The cryptic rac prophage in Escherichia coli K-12 carries the gene for a putative transcription factor RacR, whose deletion is lethal. Horizontal gene transfer is a major driving force behind the genomic diversity seen in prokaryotes.
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