subtilis and a pathogenic species.IMPORTANCE DnaB is a replicative helicase loader involved in initiating DNA replication in many bacterial species. We investigated the binding preferences of DnaB for its DNA substrate and determined that the C-terminal end of the protein plays a critical role in controlling DNA interactions. Furthermore, we found that DNA binding in general did not trigger changes to the oligomeric state of DnaB, but rather, certain types of single-stranded DNA substrates specifically induced DnaB to self-assemble into a large complex. This indicates that the structure of DNA itself is an important regulatory element that influences the behavior of DnaB. Importantly, these observations held for both Bacillus subtilis and the pathogenic species Staphylococcus aureus, demonstrating conserved biochemical functions of DnaB in these species.Magnetotactic bacteria are aquatic or sediment-dwelling microorganisms able to take advantage of the Earth's magnetic field for directed motility.  https://www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html  The source of this amazing trait is magnetosomes, unique organelles used to synthesize single nanometer-sized crystals of magnetic iron minerals that are queued up to build an intracellular compass. Most of these microorganisms cannot be cultivated under controlled conditions, much less genetically engineered, with only few exceptions. However, two of the genetically amenable Magnetospirillum species have emerged as tractable model organisms to study magnetosome formation and magnetotaxis. Recently, much has been revealed about the process of magnetosome biogenesis and dedicated structures for magnetosome dynamics and positioning, which suggest an unexpected cellular intricacy of these organisms. In this minireview, we summarize new insights and place the molecular mechanisms of magnetosome formation in the context of the complex cell biology of Magnetospirillum spp. First, we provide an overview on magnetosome vesicle synthesis and magnetite biomineralization, followed by a discussion of the perceptions of dynamic organelle positioning and its biological implications, which highlight that magnetotactic bacteria have evolved sophisticated mechanisms to construct, incorporate, and inherit a unique navigational device. Finally, we discuss the impact of magnetotaxis on motility and its interconnection with chemotaxis, showing that magnetotactic bacteria are outstandingly adapted to lifestyle and habitat.The Negativicutes are a clade of the Firmicutes that have retained the ancestral diderm character and possess an outer membrane. One of the best studied Negativicutes, Veillonella parvula, is an anaerobic commensal and opportunistic pathogen inhabiting complex human microbial communities, including the gut and the dental plaque microbiota. Whereas the adhesion and biofilm capacities of V. parvula are expected to be crucial for its maintenance and development in these environments, studies of V. parvula adhesion have been hindered by the lack of efficient genetic tools to perform functional analyses in this bacterium. Here, we took advantage of a recently described naturally transformable V. parvula isolate, SKV38, and adapted tools developed for the closely related Clostridia spp. to perform random transposon and targeted mutagenesis to identify V. parvula genes involved in biofilm formation. We show that type V secreted autotransporters, typically found in diderm bacteria, are the main determinants of V. para. Although the adhesive capacity of V. parvula has been previously described, very little is known about the underlying molecular mechanisms due to a lack of genetically amenable Veillonella strains. In this study, we took advantage of a naturally transformable V. parvula isolate and newly adapted genetic tools to identify surface-exposed adhesins called autotransporters as the main molecular determinants of adhesion in this bacterium. This work therefore provides new insights on an important aspect of the V. parvula lifestyle, opening new possibilities for mechanistic studies of the contribution of biofilm formation to the biology of this major commensal of the oral-digestive tract.Cell growth and division are coordinated, ensuring homeostasis under any given growth condition, with division occurring as cell mass doubles. The signals and controlling circuit(s) between growth and division are not well understood; however, it is known in Escherichia coli that the essential GTPase Era, which is growth rate regulated, coordinates the two functions and may be a checkpoint regulator of both. We have isolated a mutant of Era that separates its effect on growth and division. When overproduced, the mutant protein Era647 is dominant to wild-type Era and blocks division, causing cells to filament. Multicopy suppressors that prevent the filamentation phenotype of Era647 either increase the expression of FtsZ or decrease the expression of the Era647 protein. Excess Era647 induces complete delocalization of Z rings, providing an explanation for why Era647 induces filamentation, but this effect is probably not due to direct interaction between Era647 and FtsZ. The hypermorphic ftsZ* allele at the natinates this process with ribosome biogenesis.The nosocomial pathogen Clostridioides difficile is a spore-forming obligate anaerobe that depends on its aerotolerant spore form to transmit infections. Functional spore formation depends on the assembly of a proteinaceous layer known as the coat around the developing spore. In C. difficile, coat assembly depends on the conserved spore protein SpoIVA and the clostridial-organism-specific spore protein SipL, which directly interact. Mutations that disrupt their interaction cause the coat to mislocalize and impair spore formation. In Bacillus subtilis, SpoIVA is an ATPase that uses ATP hydrolysis to drive its polymerization around the forespore. Loss of SpoIVA ATPase activity impairs B. subtilis SpoIVA encasement of the forespore and activates a quality control mechanism that eliminates these defective cells. Since this mechanism is lacking in C. difficile, we tested whether mutations in the C. difficile SpoIVA ATPase motifs impact functional spore formation. Disrupting C. difficile SpoIVA ATPase motifs resulted in phenotypes that were typically >104-fold less severe than the equivalent mutations in B.