Effects of metabolic inhibitors on extracellular fructosyltransferase production in Actinomyces viscosus.
Identifieur interne : 009150 ( Ncbi/Merge ); précédent : 009149; suivant : 009151Effects of metabolic inhibitors on extracellular fructosyltransferase production in Actinomyces viscosus.
Auteurs : W. Chak ; H K KuramitsuSource :
- Infection and Immunity [ 0019-9567 ] ; 1981.
Abstract
Extracellular fructosyltransferase (levansucrase; EC 2.4.1.10) production in Actinomyces viscosus T14AV was demonstrated to occur concomitantly with cellular growth. The inhibition of both cellular ribonucleic acid and protein synthesis resulted in no further accumulation of enzyme activity. The antibiotic sodium clofibrate differentially inhibited the production of fructosyltransferase by strain T14AV. Furthermore, the antibiotic preferentially inhibited [14C]acetate incorporation into cellular lipid, but did not affect protein synthesis. In addition, no inhibition of fructosyltransferase production was observed upon the addition of the fatty acid acid synthesis inhibitor cerulenin. On the other hand, extracellular fructosyltransferase production was apparently stimulated in the presence of the cell wall synthesis inhibitors penicillin, amphomycin, and tunicamycin. These results are discussed in terms of the mechanism of extracellular protein production in A. viscosus.
Url:
PubMed: 7333676
PubMed Central: 350958
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PMC:350958Le document en format XML
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<author><name sortKey="Chak, W" sort="Chak, W" uniqKey="Chak W" first="W" last="Chak">W. Chak</name>
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<front><div type="abstract" xml:lang="en"><p>Extracellular fructosyltransferase (levansucrase; EC 2.4.1.10) production in Actinomyces viscosus T14AV was demonstrated to occur concomitantly with cellular growth. The inhibition of both cellular ribonucleic acid and protein synthesis resulted in no further accumulation of enzyme activity. The antibiotic sodium clofibrate differentially inhibited the production of fructosyltransferase by strain T14AV. Furthermore, the antibiotic preferentially inhibited [14C]acetate incorporation into cellular lipid, but did not affect protein synthesis. In addition, no inhibition of fructosyltransferase production was observed upon the addition of the fatty acid acid synthesis inhibitor cerulenin. On the other hand, extracellular fructosyltransferase production was apparently stimulated in the presence of the cell wall synthesis inhibitors penicillin, amphomycin, and tunicamycin. These results are discussed in terms of the mechanism of extracellular protein production in A. viscosus.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id>
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<title-group><article-title>Effects of metabolic inhibitors on extracellular fructosyltransferase production in Actinomyces viscosus.</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Chak</surname>
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<pub-date pub-type="ppub"><month>12</month>
<year>1981</year>
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<volume>34</volume>
<issue>3</issue>
<fpage>930</fpage>
<lpage>937</lpage>
<abstract><p>Extracellular fructosyltransferase (levansucrase; EC 2.4.1.10) production in Actinomyces viscosus T14AV was demonstrated to occur concomitantly with cellular growth. The inhibition of both cellular ribonucleic acid and protein synthesis resulted in no further accumulation of enzyme activity. The antibiotic sodium clofibrate differentially inhibited the production of fructosyltransferase by strain T14AV. Furthermore, the antibiotic preferentially inhibited [14C]acetate incorporation into cellular lipid, but did not affect protein synthesis. In addition, no inhibition of fructosyltransferase production was observed upon the addition of the fatty acid acid synthesis inhibitor cerulenin. On the other hand, extracellular fructosyltransferase production was apparently stimulated in the presence of the cell wall synthesis inhibitors penicillin, amphomycin, and tunicamycin. These results are discussed in terms of the mechanism of extracellular protein production in A. viscosus.</p>
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