107(P62) アンサマイシン系抗生物質リファマイシンの生合成 : タイプIポリケチドシンターゼによる鎖長伸長機構(ポスター発表の部)

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The assembly of the polyketide backbone of rifamycin B on the type I rifamycin polyketide synthase (PKS), encoded by the rifA-rifE genes, is terminated by the product of the rifF gene, an amide synthase that releases the completed undecaketide as its macrocyclic lactam. Inactivation of rifF gives a rifamycin B nonproducing mutant that still accumulates a series of linear polyketides ranging from the tetra- to a decaketide, also detected in the wild type, demonstrating that the PKS operates in a processive manner. Disruptions of the rifD module 8 and rifE module 9 and 10 genes also result in accumulation of such linear polyketides as a consequence of premature termination of polyketide assembly. Whereas the tetraketide carries an unmodified aromatic chromophore, the penta- through decaketide have undergone oxidative cyclization to the naphthoquinone, suggesting that this modification occurs during, not after, PKS assembly. The structure of one of the accumulated compounds together with ^<18>O experiments suggests that this oxidative cyclization produces an 8-hydroxy-7,8-dihydronaphthoquinone structure that, after the stage of proansamycin X, is dehydrogenated to an 8-hydroxynaphtoquinone. Inaction of the rifR gene that encodes a thioesterase II-like protein, both in the wild type and rifF mutant backgrounds decrease yield of rifamycin B and premature polyketides, but rifR rifF mutant still produces tetra- through decaketide, showing it is unlikely that the RifR thioesterase catalyzes their release to a major extent.
天然有機化合物討論会の論文
1999-09-01

107(P62) アンサマイシン系抗生物質リファマイシンの生合成 : タイプIポリケチドシンターゼによる鎖長伸長機構(ポスター発表の部)

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