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Amblar, M.

Publications and source records attributed to Amblar, M..

2 recordsLinked to original sources

StIA is a Novel Nucleoid-Associated Protein of Streptococcus pneumoniae that Activates DNA Topoisomerase I

Topoisomerases are essential enzymes that maintain DNA topology. The activity of some of these enzymes is regulated by protein cofactors. Here, we identify a previously uncharacterized nucleoid-associated protein from the human pathogen Streptococcus pneumoniae that binds double-stranded DNA (dsDNA) in a sequence-independent manner both in vitro and in vivo and activates topoisomerase I (Topo I). This protein was named StIA (Streptococcal Topoisomerase I Activator). In vivo analyses showed that deletion of stIA impairs bacterial growth in the presence of the Topo I inhibitor seconeolitsine, whereas its overproduction decreases susceptibility to this compound. Consistent with these observations, StIA specifically stimulates Topo I activity without affecting DNA gyrase. StIA forms oligomers and assembles into higher-order nucleoprotein complexes upon DNA-binding. Mechanistic analyses revealed that StIA does not alter DNA cleavage by Topo I but specifically enhances the DNA religation step of its catalytic cycle. This activation is likely mediated through a direct protein-protein interaction, as StIA and Topo I physically associate in vitro. Structural modeling further supports the formation of a StIA-Topo I complex and identifies putative contact residues involved in the interaction. Collectively, these findings establish StIA as a novel nucleoid-associated with a dual function: promoting nucleoprotein complex assembly and stimulating Topo I activity through direct interaction with the enzyme. More broadly, our results suggest that the regulation of topoisomerase activity by accessory proteins may represent an important mechanism for fine-tuning DNA topological homeostasis and could provide new opportunities for the development of antibacterial therapies.

microbiology↗

RNase R Controls Membrane Fatty Acid Composition in Streptococcus pneumoniae

AO_SCPLOWBSTRACTC_SCPLOWPrevious studies on RNase R have highlighted significant effects of this ribonuclease in several processes of Streptococcus pneumoniae biology. In this work we have studied the global impact of RNase R by comparing the transcriptional landscape of a deleted RNase R mutant to that of the wild-type strain, and this led us investigate specific targets affected by RNase R. RNA-Seq showed that RNase R deletion affects transcripts from several different biological processes. Of particular interest, elimination of RNase R results in overexpression of most of the genes encoding the components of type II fatty acid biosynthesis (FAS-II) cluster. We demonstrate that RNase R governs the turnover of most of genes from this pathway, affecting the outcome of the whole FAS-II cluster, and leading to an unbalanced membrane fatty acid composition. Our results show that the membrane of the deleted strain contains a higher proportion of unsaturated and long-chained fatty acids than the wild type strain. This leads to a higher fluidity of the {Delta}rnr mutant membrane, which is probably related with the increased sensitivity to detergent observed in this strain. We demonstrate that RNase R expression is induced in cells challenged with H2O2, which is suggestive of a role for this ribonuclease on the regulation of membrane homeostasis under oxidative stress. Reprogramming of membrane fluidity is an adaptative cell response crucial for bacterial survival in constantly changing environmental conditions. The fact that RNase R controls the expression of several essential genes to the fatty acid synthesis unveils a new important function of this enzyme.

molecular biology↗