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Transcriptionally Regulatory Sequences of Phylogenetic Significance
Published in S. K. Dutta, DNA Systematics, 2019
DNA sequences signaling the end of a gene function terminate transcription at the proper site of their transcriptional unit, thus allowing independent transcription of their adjacent genes. With this signal, RNA chain elongation ceases, the transcript is released, and the polymerase is dissociated from the template. At least two classes of such sequences have been identified, specific rho factor (a) dependent or (b) independent. In prokaryotes, rho factor-dependent termination occurs near the 3′ end of a coding sequence which is recognized by a protein factor, rho (ρ), about 46,000 in mol wt. ρ acts through its single-stranded, RNA-dependent ATP nucleoside triphosphate phosphohydrolase activity and may assume altered conformations when bound to a nucleotide substrate or product.229 Its functional form is probably a hexamer. The sequence of the ρ gene has recently been determined.230
Riboswitches as therapeutic targets: promise of a new era of antibiotics
Published in Expert Opinion on Therapeutic Targets, 2023
Emily Ellinger, Adrien Chauvier, Rosa A. Romero, Yichen Liu, Sujay Ray, Nils G. Walter
Recent studies have unveiled additional mechanisms of gene regulation that are mediated by riboswitches in response to their ligand and could be exploited for the design of more specific drugs targeting a specific bacterial phylum or species [74,75] (Figure 5). For instance, the TPP, FMN, and magnesium-sensing riboswitches have been found to trigger transcription termination in response to their respective ligands through the Rho transcription factor [76–78] (Figure 5(a)). Since this mechanism involves the sequestration or accessibility of the Rho binding site (i.e. Rho utilization site or rut sequence) as a function of riboswitch folding, it contrasts with polarity regulation in which the absence of translation of the nascent mRNA allows Rho-dependent transcription termination [30]. Bicyclomycin is a compound that specifically inhibits Rho activity [79,80], however, because of its low specificity toward a particular bacterial phylum, future avenues are needed that target Rho factor only in pathogenic bacteria and not in the commensal, beneficial species found in the human gut microbiome [81,82].