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This study demonstrates that infection by pathogenic bacteria (Staphylococcus aureus and Pseudomonas aeruginosa) or hypoxic conditions trigger reorganization of the mitochondrial network in the roundworm Caenorhabditis elegans. The researchers identified that genes involved in lysosome-related organelles (LROs) are essential for this mitochondrial remodeling process and also drive the expression of infection-response genes. The findings reveal a previously unknown mechanism linking lysosomal components to mitochondrial changes during bacterial infection.
Why it matters
Understanding how cells detect and respond to bacterial pathogens through mitochondrial changes could inform new therapeutic strategies for treating bacterial infections. Since mitochondria contain resources that bacteria need for growth, clarifying the cellular mechanisms that protect mitochondria during infection may lead to novel approaches for enhancing host immunity.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Detecting and responding to pathogenic bacteria is an essential function of eukaryotic cells. As bacteria-derived organelles, mitochondria carry lipids, proteins, and other molecules such as iron which are required for bacterial growth, and thus are subject to pathogenic bacterial attack. In fact, mitochondrial morphology and function are often altered during early bacterial infection. However, the mechanism by which bacterial pathogen attack triggers mitochondrial responses is unknown. Here, we demonstrate that infection by the pathogenic bacterium Staphylococcus aureus or Pseudomonas aeruginosa or hypoxia leads to remodeling of the mitochondrial network in the host Caenorhabditis elegans. Our analysis discovers that lysosome-related organelle (LRO) genes are required for this remodeling and indicates that LROs also precipitate downstream infection-response gene expression.