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Listeria monocytogenes upregulates mitochondrial calcium signalling to inhibit LC3-associated phagocytosis as a survival strategy
Nat Microbiol.2021-01;
Tianliang Li, Ligang Kong, Xinghui Li, Sijin Wu, Kuldeep S Attri, Yan Li, Weipeng Gong, Bao Zhao, Lupeng Li, Laura E Herring, John M Asara, Lei Xu, Xiaobo Luo, Yu L Lei, Qin Ma, Stephanie Seveau, John S Gunn, Xiaolin Cheng, Pankaj K Singh, Douglas R Green, Haibo Wang, Haitao Wen
… -GFP (sc-9996) and anti-Actin (sc-1615) from Santa Cruz Biotechnology; anti-GILT (HM-1128)
from Hycult Biotech; anti-Unc93b antibody (PRS4553), anti-FLAG M2-HRP (A8592) and anti-HA-HRP
(11667475001) from Sigma–Aldrich; and anti-V5-HRP (A00877) from GenScript. …
Mitochondria are believed to have originated ~2.5 billion years ago. As well as energy generation in cells, mitochondria have a role in defence against bacterial pathogens. Despite profound changes in mitochondrial morphology and functions following bacterial challenge, whether intracellular bacteria can hijack mitochondria to promote their survival remains elusive. We report that Listeria monocytogenes-an intracellular bacterial pathogen-suppresses LC3-associated phagocytosis (LAP) by modulation of mitochondrial Ca (mtCa) signalling in order to survive inside cells. Invasion of macrophages by L. monocytogenes induced mtCa uptake through the mtCa uniporter (MCU), which in turn increased acetyl-coenzyme A (a... More
Mitochondria are believed to have originated ~2.5 billion years ago. As well as energy generation in cells, mitochondria have a role in defence against bacterial pathogens. Despite profound changes in mitochondrial morphology and functions following bacterial challenge, whether intracellular bacteria can hijack mitochondria to promote their survival remains elusive. We report that Listeria monocytogenes-an intracellular bacterial pathogen-suppresses LC3-associated phagocytosis (LAP) by modulation of mitochondrial Ca (mtCa) signalling in order to survive inside cells. Invasion of macrophages by L. monocytogenes induced mtCa uptake through the mtCa uniporter (MCU), which in turn increased acetyl-coenzyme A (acetyl-CoA) production by pyruvate dehydrogenase. Acetylation of the LAP effector Rubicon with acetyl-CoA decreased LAP formation. Genetic ablation of MCU attenuated intracellular bacterial growth due to increased LAP formation. Our data show that modulation of mtCa signalling can increase bacterial survival inside cells, and highlight the importance of mitochondrial metabolism in host-microbial interactions.