Biological properties and mode of action of clavams.
The clavams valclavam and hydroxyethylclavam were both bacteriostatic and fungistatic. The molecular basis for growth inhibition of Escherichia coli was a non-competitive inhibition of homoserine-O-succinyltransferase (EC 2.3.1.46), thus blocking methionine biosynthesis. Eucaryotes such as Saccharomyces cerevisiae were inhibited by a different mode of action. Instead of interfering with methionine biosynthesis, the clavams inhibited the formation of RNA in living cells, although the RNA-polymerases of isolated yeast nuclei were not inhibited. The action of valclavam on E. coli was dependent on functional peptide transport systems.
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Rabenhorst
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D000217:Acyltransferases / Q000037:antagonists & inhibitors; D001419:Bacteria / Q000187:drug effects*; D001692:Biological Transport; D004271:DNA, Fungal / Q000096:biosynthesis; D004926:Escherichia coli / Q000187:drug effects / Q000201:enzymology; D005658:Fungi / Q000187:drug effects*; D051082:Homoserine O-Succinyltransferase; D008997:Monobactams / Q000494:pharmacology*; D009089:Mucor / Q000187:drug effects; D010455:Peptides / Q000378:metabolism / Q000494:pharmacology; D012331:RNA, Fungal / Q000096:biosynthesis; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000378:metabolism
D004271:DNA, Fungal; D008997:Monobactams; D010455:Peptides; D012331:RNA, Fungal; C053058:hydroxyethylclavam; C053057:valclavam; D000217:Acyltransferases; D051082:Homoserine O-Succinyltransferase