ArticleInfection and immunity1995
The two distinct phospholipases C of Listeria monocytogenes have overlapping roles in escape from a vacuole and cell-to-cell spread.
Article in Infection and immunity, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.
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Who cites it
200 citing papers in PubMed, 448 citations in OpenAlex.
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- Soil microbial responses to multiple global change factors as assessed by metagenomics.Nature communications · 2025Article
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- Executioner caspases degrade essential mediators of pathogen-host interactions to inhibit growth of intracellular Listeria monocytogenes.Cell death & disease · 2025Article
- Pathogenic rickettsiae encode a secreted lipase that facilitates intracytosolic colonization in host cells.PloS one · 2025Article
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Investigation on the inactivation effect and mechanism of Listeria monocytogenes in fresh-cut cucumber during storage by ultrasound combined with sodium hypochlorite.Ultrasonics sonochemistry · 2023Article
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- Structural basis for the unique molecular properties of broad-range phospholipase C from Listeria monocytogenes.Nature communications · 2023Article
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- Human Listeriosis.Clinical microbiology reviews · 2023Review
- TargeTron inactivation of plasmid-regulated Chlamydia trachomatis CT084 results in a nonlytic phenotype.Pathogens and disease · 2023Article
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- The patatin-like phospholipaseFrontiers in cellular and infection microbiology · 2023Article
- Phospholipase C: underrated players in microbial infections.Frontiers in cellular and infection microbiology · 2023Review
140 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Listeria monocytogenes secretes two distinct phospholipases C, a phosphatidylinositol-specific phospholipase C (PI-PLC) and a broad-range phospholipase C (PC-PLC). In this study, single in-frame deletion mutants with mutations in each PLC and a double mutant lacking both PLCs were characterized with regard to virulence in mice, escape from a primary vacuole, and cell-to-cell spread in cell culture. The mutant lacking PI-PLC, previously shown to be twofold less virulent than the wild type in mice, had a minor defect in escape from a primary vacuole but was not notably affected in cell-to-cell spread. The mutant lacking PC-PLC was 20-fold less virulent in mice and was defective in cell-to-cell spread but had no measurable defect in escape from a primary vacuole. The mutant lacking both PLCs was 500-fold less virulent in mice and was severely diminished in its ability to escape from the primary vacuole and to spread cell to cell. Cellular levels of diacylglycerol and ceramide, products of PLC activity, accumulated beginning 3 to 4 h after infection of cells with wild-type bacteria. The bacterial PLCs were partially responsible for this activity, since cells infected with the mutant lacking both PLCs had a reduced increase in diacylglycerol and no increase in ceramide. Elevation of diacylglycerol in the absence of bacterial PLCs indicated that host cell phospholipase(s) was activated during infection. The results of this study were consistent with the two bacterial PLCs having overlapping functions throughout the course of intracellular infection. Furthermore, the PC-PLC, and possibly PI-PLC, appeared to be enzymatically active intracellularly.
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