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Transcriptionally Regulatory Sequences of Phylogenetic Significance
Published in S. K. Dutta, DNA Systematics, 2019
Escherichia coli is a natural host for bacteriophage. As has been amply documented, its RNA polymerase is larger and more complex than that of the phage, consisting of several subunits (α2, β, βʹ) totaling about 355,000 daltons.2 The precise recognition of promoters by this core polymerase requires an additional polypeptide, the sigma factor. Together, these polypeptide units constitute the polymerase holoenzyme.
Arcobacter
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Nuria Salas-Massó, Alba Perez-Cataluña, Luis Collado, Arturo Levican, Maria José Figueras
Flagellin genes are related with flagellum and, therefore, with the capacity of infection and invasion. In this regard, alterations in the flaB gene in one strain of A. butzleri did not influence the formation of the flagella, but mutations in the flaA gene can produce a loss of flagella and of motility [1 and references therein]. It has been observed that the genome of A. butzleri RM4018 carries genes for the flagella structure; however, some of the genes involved in the regulation of flagella transcription typically found in other Epsilonbacteria like flgM gene or the sigma factor gene rpoN, were not present. Nevertheless, it has been indicated that the presence of other sigma factor genes present in that genome could compensate for the functions of the missing genes [57].
Clostridium difficile
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
Low levels of biotin also increase toxin production. During exponential growth, TcdC is high and it is believed to be an anti-sigma factor negatively regulating toxin production. TcdC mutants have been described. These strains produce increased amounts of toxins A and B in vitro, particularly in stationary phase. These mutant strains appear to be particularly virulent. TcdD is not an exotoxin per se, but a positive regulator of transcription of toxin genes and is also responsible for the temperature-dependent regulation of toxin production. The sigma factor TcdR is also a positive regulator, although it is itself under some form of regulation. Additionally, C. difficile has a luxS-type quorum-sensing signaling system, although evidence suggests that addition of the inducer (AI-2) has no effect on toxin production.
Regulation of flagellar motility and biosynthesis in enterohemorrhagic Escherichia coli O157:H7
Published in Gut Microbes, 2022
Hongmin Sun, Min Wang, Yutao Liu, Pan Wu, Ting Yao, Wen Yang, Qian Yang, Jun Yan, Bin Yang
In E. coli, including EHEC O157:H7, the expression of flagellar genes is a tightly regulated and highly energetic three-tier process (Figure 3).12 The Class I gene flhDC encodes proteins FlhD and FlhC, that assemble into the heterohexamer (FlhD4C2).14 The FlhD4C2 proteins complex binds to the DNA upstream of Class II genes, recruits RNA polymerase, and promotes σ70-dependent transcription (Figure 3).17 FliA is an alternate sigma factor (σ28), encoded by a Class II gene, specifically required for transcription initiation of Class III genes.18 FlgM acts as an anti-sigma factor that binds to FliA directly, preventing interaction with RNA polymerase and repressing FliA-dependent transcription until after hook-basal body are formed.19 Upon assembly of the basal body and secretion apparatus, FlgM is exported out of the cell, freeing FliA and allowing initiation of FliA-dependent transcription from Class III promoters.20 This three-tiered flagellar regulatory cascade helps bacteria, including EHEC O157:H7, to conserve biosynthetic resources and ensure the efficiency of flagellar assembly.
The ancestral stringent response potentiator, DksA has been adapted throughout Salmonella evolution to orchestrate the expression of metabolic, motility, and virulence pathways
Published in Gut Microbes, 2022
Helit Cohen, Boaz Adani, Emiliano Cohen, Bar Piscon, Shalhevet Azriel, Prerak Desai, Heike Bähre, Michael McClelland, Galia Rahav, Ohad Gal-Mor
Changes in the DksA regulatory setup may have evolved by adaptation of newly acquired promoters to facilitate direct binding of an RNAP-DksA complex. For example, our results support the possibility that a DksA-RNAP complex binds at the regulatory region of hilA, the SPI-1 master regulator, and by that mechanism may affect the transcription of the entire SPI-1 regulon. Nonetheless, additional experimental approaches, such as in-vitro transcription, are needed to further confirm this possibility. Another indirect mechanism responsible for changes in the DksA regulon might be changes in the expression pattern of other global regulators, downstream to DksA. For example, we found that the lack DksA, leads to a significant increase in the expression of the flagellar sigma factor fliA (sigma 28) in E. coli, but not in Salmonella spp. (Figure 10 and Fig. S7A), explaining the increased expression of motility and chemotaxis genes in this species. In contrast, the lack of DksA resulted in a very prominent decrease in the expression of the stress response sigma factor, RpoS (sigma 38) in E. coli, while the expression of RpoS was not significantly affected in Salmonella Typhimurium grown to the late logarithmic phase (Fig. S7). Furthermore, the expression of the alternative sigma factor rpoE (sigma 24) was also found to significantly decrease in the absence of DksA in both Salmonella species, but not in E. coli (Fig. S7A). Therefore, these differences can contribute to changes in the expression of RpoE- and RpoS-regulated genes in an indirect DksA-dependent manner.
Epithelial damage in the cystic fibrosis lung: the role of host and microbial factors
Published in Expert Review of Respiratory Medicine, 2022
Arlene M. A. Glasgow, Catherine M. Greene
Chronically adapted P. aeruginosa strains are often found to express mutations that cause hyper production of exopolysaccharides, the most notable of these being alginate. In wild-type P. aeruginosa, alginate synthesis is inactive due to the sequestering of the sigma factor AlgT by MucA. The spontaneous acquisition of mucA mutations results in dysfunctional MucA protein and therefore the release of AlgT, which can then initiate transcription at the alginate biosynthesis operon [38]. Overproduction of alginate signifies the conversion of P. aeruginosa to a mucoid phenotype, which is highly resistant to antibiotic treatment and is rarely eradicated from the CF airway once established. The mucoid phenotype of P. aeruginosa is associated with worse clinical outcomes, e.g. severe bronchiectasis, faster decline in lung function, and increased mortality [39]. Indeed, multiple drug resistant P. aeruginosa belonging to different clades can co-exist in the lungs of people with CF, and the CF lung milieu actually provides an environment that drives adaptations in P. aeruginosa as shown by whole genome sequencing [40,41].