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Inhibition of Trichothecin and Ergosterol Biosynthesis in Trichothecium roseum by Lovastatin
Author(s) -
Huang WanLing,
Lee Kuan Rong,
Shiao MingShi
Publication year - 1999
Publication title -
journal of the chinese chemical society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.329
H-Index - 45
eISSN - 2192-6549
pISSN - 0009-4536
DOI - 10.1002/jccs.199900094
Subject(s) - lovastatin , chemistry , ergosterol , mevalonic acid , reductase , biochemistry , biosynthesis , hmg coa reductase , cholesterol , enzyme
The effect of lovastatin, an HMG‐CoA reductase inhibitor, on the biosynthesis of trichothecin, ergosterol, and fatty acids in the fungus Trichothecium roseum was investigated. Treatment of lovastatin (50 μM) to a 5‐day‐old culture of T. roseum reduced the incorporation of [2‐ 14 C]acetate into trichothecin by 79%, whereas the conversion of [5‐ 3 H]mevalonate into this sesquiterpenoid mycotoxin was reduced by only 28%. In a parallel experiment, the incorporation of [2‐ 14 C]acetate and [5‐ 3 H]mevalonate into ergosterol were decreased by 78% and 17%, respectively. Meanwhile, the conversion of labeled acetate into fatty acids was not significantly affected. These results indicate that HMG‐CoA reductase is a major, but not strict, regulatory site in mevalonic acid pathway leading to the formation of trichothecin and ergosterol. No priority was found in utilization of a single, residual mevalonic acid pool in response to lovastatin inhibition for the biosynthesis of trichothecin and ergosterol. Inhibition of mevalonic acid formation does not significantly divert acetyl CoA into fatty acid synthesis.