Inactivation of urea-treated phage T4 by phosphatidylglycerol

Urea-treated phage T4 infection of Escherichia coli B/4 spheroplasts is inhibited by spheroplast debris. Almost all the inhibitory activity is due to phosphatidylglycerol (PG), one of the three major phospholipids of the cell. Neither phosphatidylethanolamine nor cardiolipin, the other major phospho...

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Veröffentlicht in:Virology (New York, N.Y.) N.Y.), 1970-06, Vol.41 (2), p.356-364
Hauptverfasser: Baumann, Linda, Benz, Wendy C., Wright, A., Goldberg, Edward B.
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Sprache:eng
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Zusammenfassung:Urea-treated phage T4 infection of Escherichia coli B/4 spheroplasts is inhibited by spheroplast debris. Almost all the inhibitory activity is due to phosphatidylglycerol (PG), one of the three major phospholipids of the cell. Neither phosphatidylethanolamine nor cardiolipin, the other major phospholipids, show significant inhibitory activity. PG from both Salmonella and Staphylococcus inhibits infection to the same degree. It has no effect on normal T4 infection of E. coli B cells. Electron micrographs of urea-treated phage preparations indicate that phosphatidylglycerol causes about 50% of the phage particles to lose their DNA and also brings about significant clumping of phage particles. These findings indicate that PG might either play a role as the urea-treated phage receptor on the spheroplast surface or it might act as a trigger causing release of DNA from the phage.
ISSN:0042-6822
1096-0341
DOI:10.1016/0042-6822(70)90088-7