RNase R is a processive 3'-5' exoribonuclease with a high degree of conservation in prokaryotes. Although some bacteria possess additional hydrolytic 3'-5' exoribonucleases such as RNase II, RNase R was found to be the only predicted one in the facultative intracellular pathogen Legionella pneumophila. This provided a unique opportunity to study the role of RNase R in the absence of an additional RNase with similar enzymatic activity. We investigated the role of RNase R in the biology of Legionella pneumophila under various conditions and performed gene expression profiling using microarrays. At optimal growth temperature, the loss of RNase R had no major consequence on bacterial growth and had a moderate impact on normal gene regulation. However, at a lower temperature, the loss of RNase R had a significant impact on bacterial growth and resulted in the accumulation of structured RNA degradation products. Concurrently, gene regulation was affected and specifically resulted in an increased expression of the competence regulon. Loss of the exoribonuclease activity of RNase R was sufficient to induce competence development, a genetically programmed process normally triggered as a response to environmental stimuli. The temperature-dependent expression of competence genes in the rnr mutant was found to be independent of previously identified competence regulators in Legionella pneumophila. We suggest that a physiological role of RNase R is to eliminate structured RNA molecules that are stabilized by low temperature, which in turn may affect regulatory networks, compromising adaptation to cold and thus resulting in decreased viability.
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http://dx.doi.org/10.1128/JB.01035-08 | DOI Listing |
Microorganisms
December 2024
School of Life Sciences, University of Essex, Wivenhoe Park, Colchester, CO4 3SQ, UK.
Multiple human and plant pathogens are dispersed and transmitted as bioaerosols (e.g., , SARS-CoV-2, , , spp.
View Article and Find Full Text PDFAntibiotics (Basel)
November 2024
Laboratory of Microbiology, Nova Medical School, Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal.
Background: species are the causative agent of Legionnaires' disease and, as ubiquitous waterborne bacteria, are prone to antimicrobial resistance gene (ARG) acquisition and dissemination due to the antimicrobial contamination of natural environments. Given the potential health risks associated with ARGs, it is crucial to assess their presence in the population.
Methods: The ARGs and were detected in 348 samples, isolates, and DNA extracts using conventional PCR.
Front Immunol
January 2025
Centro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mexico.
Pathogenic bacteria trigger complex molecular interactions in hosts that are characterized mainly by an increase in reactive oxygen species (ROS) as well as an inflammation-associated response. To counteract oxidative damage, cells respond through protective mechanisms to promote resistance and avoid tissue damage and infection; among these cellular mechanisms the activation or inhibition of the nuclear factor E2-related factor 2 (Nrf2) is frequently observed. The transcription factor Nrf2 is considered the regulator of several hundred cytoprotective and antioxidant genes.
View Article and Find Full Text PDFMucosal Immunol
December 2024
Department of Infectious Diseases, Respiratory Medicine and Critical Care, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, 13353 Berlin, Germany; German center for lung research (DZL), Augustenburger Platz 1, 13353 Berlin, Germany. Electronic address:
Diabetes mellitus is associated with an increased risk of pneumonia, often caused by so-called typical and atypical pathogens including Streptoccocus pneumoniae and Legionella pneumophila, respectively. Here, we employed a variety of mouse models to investigate how diabetes influences pulmonary antibacterial immunity. Following intranasal infection with S.
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