Seminar Series – 16 Dec
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SymbNET Online Seminar Series
Monthly seminars on host-microbe symbiosis, genomics, and metabolomics, with two talks from SymbNET researchers.
The seminars are open and free to all, but registration is required.
Please register once for the entire seminar series.
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15:00 WET / 16:00 CET
Affiliation: Systems Microbiology Lab, EMBL, Germany
Title: A tripartite toxin-antitoxin system sensing and defending phage.
Abstract: Retrons are genetic retroelements, commonly found in bacterial genomes and recently repurposed as genome editing tools. Their encoded reverse transcriptase (RT) produces a multi-copy single-stranded DNA (msDNA). Despite our understanding of their complex biosynthesis, the function of msDNAs and therefore, the physiological role of retrons has remained elusive. We have recently established that the Retron-Sen2 in Salmonella Typhimurium encodes a novel family of tripartite toxin/antitoxin systems, which is activated during phage infection to protect against phages through abortive infection.
15:30 WET / 16:30 CET
Affiliation: Innate Immunity and Inflammation, FCG-IGC, Portugal
Title: Induction of immune responses by surveillance of homeostasis perturbations.
Abstract: Several classes of antibiotics have long been known to have beneficial effects that cannot be explained strictly on the basis of their capacity to control the infectious agent. We found that tetracycline antibiotics, which target the mitoribosome, protected against sepsis, without affecting the pathogen load. Mechanistically, we demonstrate that mitochondrial inhibition of protein synthesis perturbed the electron transfer chain (ETC) decreasing tissue damage in the lung and increasing fatty acid oxidation and glucocorticoid sensitivity in the liver. Using a liver-specific partial and acute deletion of Crif1, a critical mitoribosomal component for protein synthesis, we found that mice were protected against sepsis, an observation which was phenocopied by the transient inhibition of complex I of the ETC by phenformin. Together, we demonstrate that mitoribosome-targeting antibiotics are beneficial beyond their antibacterial activity and that mitochondrial protein synthesis inhibition leading to ETC perturbation is a mechanism for the induction of disease tolerance.
SymbNET Seminars