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Gene Review

plc  -  phospholipase C

Clostridium perfringens str. 13

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Disease relevance of plc


High impact information on plc


Chemical compound and disease context of plc


Biological context of plc

  • Another variable region spanning the major virulence gene plc, which encodes the cytolytic toxin, alpha, was located near oriC in all cases whereas the gene for another lethal typing toxin, epsilon, was borne by an episome [14].
  • Comparison of the nucleotide sequence between the 3.1-kb fragments of the two type strains shows some differences both in the plc gene and in ORF2 [3].
  • However, one of these proteins, which binds within the plc coding region, was not found in the type C strain, suggesting that it plays a role in the regulation of the plc gene expression [3].
  • No significant difference in the nucleotide sequence of the plc promoter region was observed for any of the plc genes [15].
  • The deduced amino acid sequence consists of 398 amino acid residues, coinciding with those of the plc genes previously determined [16].

Anatomical context of plc


Associations of plc with chemical compounds

  • The production of chloramphenicol acetyltransferase in C. perfringens was monitored during growth and the pattern of expression was shown to reflect levels of plc mRNA and alpha-toxin in the parent strain [21].
  • However, neither phospholipase C nor 1-oleoyl-2-acetylglycerol enhanced attachment of P-29 cells or their lung-colonizing ability [9].
  • Activities of choline kinase, choline phosphotransferase, glycerol-3-phosphate dehydrogenase, glycerol-3-phosphate acyltransferase, acylglycerol-3-phosphate acyltransferase, and phosphatidic acid phosphatase in phospholipase C-treated cells were the same or only slightly higher than in control cells [22].
  • Levels of phosphocholine decreased and levels of CDP-choline increased in phospholipase C-treated cells, and a calculation of the disequilibrium ratio indicated that the cytidylyltransferase reaction was not at equilibrium [22].
  • Further experiments with genetically engineered C. perfringens PLC variants showed that the sphingomyelinase activity and the C-domain are required for its cytotoxic effect in UDP-glucose-deficient cells [11].

Regulatory relationships of plc


Other interactions of plc

  • We found that the small 3'-portion of VR-RNA was sufficient for the activation of toxin genes, which suggested that VR-RNA itself could act as an RNA regulatory molecule for the plc and colA genes mediating the regulatory information from the VirR/VirS system in C. perfringens [24].
  • The subsequent strain was complemented with separate plasmids that carried the alpha-toxin structural gene (plc), the perfringolysin O gene (pfoA), or both toxin genes, and the resultant isogenic strains were examined in a mouse myonecrosis model [25].
  • In contrast, recombination was found to be a significant factor only for the virulence genes plc and colA and the housekeeping gene gyrA [26].
  • Exogenous phospholipase C from Clostridium perfringens, at low concentrations, inactivated glycogen synthase and increased DAG without affecting cell Ca2+ or phosphorylase [23].

Analytical, diagnostic and therapeutic context of plc

  • Northern blot analysis revealed that the type A strain produced 16 to 23 times more plc mRNA than the type C strain [3].
  • Western blot analysis showed no production of alpha toxin protein in the culture supernatant of the plc mutant [5].
  • Addition of an alphatoxin (plc) gene specific PCR as an in process control reaction was performed in order to prevent false negative PCR results [27].
  • PCR analysis of 477 colonies of fecal spore isolates, from 159 patients who had a spore count > or = 10(3) cfu/g, gave positive plc gene detection in 436 colonies [28].
  • Removal of phospholipase C from the cell cultures resulted in a return to basal levels of incorporation of [3H]choline into phosphatidylcholine, a decrease in the activity of cytidylyltransferase, and a loss of the membrane-bound form of the enzyme [20].


  1. A cellular deficiency of gangliosides causes hypersensitivity to Clostridium perfringens phospholipase C. Flores-Díaz, M., Alape-Girón, A., Clark, G., Catimel, B., Hirabayashi, Y., Nice, E., Gutiérrez, J.M., Titball, R., Thelestam, M. J. Biol. Chem. (2005) [Pubmed]
  2. Virulence studies on chromosomal alpha-toxin and theta-toxin mutants constructed by allelic exchange provide genetic evidence for the essential role of alpha-toxin in Clostridium perfringens-mediated gas gangrene. Awad, M.M., Bryant, A.E., Stevens, D.L., Rood, J.I. Mol. Microbiol. (1995) [Pubmed]
  3. Comparison of the alpha-toxin genes of Clostridium perfringens type A and C strains: evidence for extragenic regulation of transcription. Katayama, S., Matsushita, O., Minami, J., Mizobuchi, S., Okabe, A. Infect. Immun. (1993) [Pubmed]
  4. Role of alpha-toxin in Clostridium perfringens infection determined by using recombinants of C. perfringens and Bacillus subtilis. Ninomiya, M., Matsushita, O., Minami, J., Sakamoto, H., Nakano, M., Okabe, A. Infect. Immun. (1994) [Pubmed]
  5. Construction of an alpha toxin gene knockout mutant of Clostridium perfringens type A by use of a mobile group II intron. Chen, Y., McClane, B.A., Fisher, D.J., Rood, J.I., Gupta, P. Appl. Environ. Microbiol. (2005) [Pubmed]
  6. Alpha toxin from Clostridium perfringens induces proinflammatory changes in endothelial cells. Bunting, M., Lorant, D.E., Bryant, A.E., Zimmerman, G.A., McIntyre, T.M., Stevens, D.L., Prescott, S.M. J. Clin. Invest. (1997) [Pubmed]
  7. Promoter upstream bent DNA activates the transcription of the Clostridium perfringens phospholipase C gene in a low temperature-dependent manner. Katayama, S., Matsushita, O., Jung, C.M., Minami, J., Okabe, A. EMBO J. (1999) [Pubmed]
  8. Phorbol esters, phospholipase C, and growth factors rapidly stimulate the phosphorylation of a Mr 80,000 protein in intact quiescent 3T3 cells. Rozengurt, E., Rodriguez-Pena, M., Smith, K.A. Proc. Natl. Acad. Sci. U.S.A. (1983) [Pubmed]
  9. Effects of 12-O-tetradecanoylphorbol-13-acetate on adhesiveness and lung-colonizing ability of Lewis lung carcinoma cells. Takenaga, K., Takahashi, K. Cancer Res. (1986) [Pubmed]
  10. Intracellular processing of cytidylyltransferase in Krebs II cells during stimulation of phosphatidylcholine synthesis. Evidence that a plasma membrane modification promotes enzyme translocation specifically to the endoplasmic reticulum. Tercé, F., Record, M., Ribbes, G., Chap, H., Douste-Blazy, L. J. Biol. Chem. (1988) [Pubmed]
  11. UDP-glucose deficiency causes hypersensitivity to the cytotoxic effect of Clostridium perfringens phospholipase C. Flores-Díaz, M., Alape-Girón, A., Titball, R.W., Moos, M., Guillouard, I., Cole, S., Howells, A.M., von Eichel-Streiber, C., Florin, I., Thelestam, M. J. Biol. Chem. (1998) [Pubmed]
  12. Lipid vesicle fusion induced by phospholipase C activity in model bile. Little, T.E., Madani, H., Lee, S.P., Kaler, E.W. J. Lipid Res. (1993) [Pubmed]
  13. A transient increase in diacylglycerols is associated with the action of vasopressin on hepatocytes. Hughes, B.P., Rye, K.A., Pickford, L.B., Barritt, G.J., Chalmers, A.H. Biochem. J. (1984) [Pubmed]
  14. Genomic diversity and organization of virulence genes in the pathogenic anaerobe Clostridium perfringens. Canard, B., Saint-Joanis, B., Cole, S.T. Mol. Microbiol. (1992) [Pubmed]
  15. Phylogenetic analysis of phospholipase C genes from Clostridium perfringens types A to E and Clostridium novyi. Tsutsui, K., Minami, J., Matsushita, O., Katayama, S., Taniguchi, Y., Nakamura, S., Nishioka, M., Okabe, A. J. Bacteriol. (1995) [Pubmed]
  16. Analysis of the phospholipase C gene of Clostridium perfringens KZ1340 isolated from Antarctic soil. Kameyama, K., Matsushita, O., Katayama, S., Minami, J., Maeda, M., Nakamura, S., Okabe, A. Microbiol. Immunol. (1996) [Pubmed]
  17. Human neutrophil peptide receptors: mobilization mediated by phospholipase C. Nelson, R.D., Fiegel, V.D., Chenoweth, D.E. Am. J. Pathol. (1982) [Pubmed]
  18. Regulation of phosphatidylcholine biosynthesis in mammalian cells. I. Effects of phospholipase C treatment on phosphatidylcholine metabolism in Chinese hamster ovary cells and LM mouse fibroblasts. Sleight, R., Kent, C. J. Biol. Chem. (1983) [Pubmed]
  19. Activation of glucose transport in skeletal muscle by phospholipase C and phorbol ester. Evaluation of the regulatory roles of protein kinase C and calcium. Henriksen, E.J., Rodnick, K.J., Holloszy, J.O. J. Biol. Chem. (1989) [Pubmed]
  20. Regulation of phosphatidylcholine biosynthesis in mammalian cells. II. Effects of phospholipase C treatment on the activity and subcellular distribution of CTP:phosphocholine cytidylyltransferase in Chinese hamster ovary and LM cell lines. Sleight, R., Kent, C. J. Biol. Chem. (1983) [Pubmed]
  21. The construction of a reporter system and use for the investigation of Clostridium perfringens gene expression. Bullifent, H.L., Moir, A., Titball, R.W. FEMS Microbiol. Lett. (1995) [Pubmed]
  22. Regulation of phosphatidylcholine biosynthesis in cultured chick embryonic muscle treated with phospholipase C. Sleight, R., Kent, C. J. Biol. Chem. (1980) [Pubmed]
  23. Mechanism of hepatic glycogen synthase inactivation induced by Ca2+-mobilizing hormones. Studies using phospholipase C and phorbol myristate acetate. Blackmore, P.F., Strickland, W.G., Bocckino, S.B., Exton, J.H. Biochem. J. (1986) [Pubmed]
  24. Clostridial VirR/VirS regulon involves a regulatory RNA molecule for expression of toxins. Shimizu, T., Yaguchi, H., Ohtani, K., Banu, S., Hayashi, H. Mol. Microbiol. (2002) [Pubmed]
  25. Synergistic effects of alpha-toxin and perfringolysin O in Clostridium perfringens-mediated gas gangrene. Awad, M.M., Ellemor, D.M., Boyd, R.L., Emmins, J.J., Rood, J.I. Infect. Immun. (2001) [Pubmed]
  26. Analysis of Core Housekeeping and Virulence Genes Reveals Cryptic Lineages of Clostridium perfringens That Are Associated With Distinct Disease Presentations. Rooney, A.P., Swezey, J.L., Friedman, R., Hecht, D.W., Maddox, C.W. Genetics (2006) [Pubmed]
  27. Controlled multiplex PCR of enterotoxigenic Clostridium perfringens strains in food samples. Schoepe, H., Potschka, H., Schlapp, T., Fiedler, J., Schau, H., Baljer, G. Mol. Cell. Probes (1998) [Pubmed]
  28. PCR detection and prevalence of enterotoxin (cpe) gene in Clostridium perfringens isolated from diarrhea patients. Tansuphasiri, U., Wongsuvan, G., Eampokalap, B. Journal of the Medical Association of Thailand = Chotmaihet thangphaet. (2002) [Pubmed]
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