Inhibition by mevinolin of plant growth, sterol formation and pigment accumulation

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Abstract
To obtain information on the importance of a functional mevalonate synthesis for plant growth and development, we investigated the effect of mevinolin, a highly specific inhibitor of 3‐hydroxy‐3‐methylglutaryl (HMG) coenzyme A reductase (the mevalonate‐producing enzyme) on growth, sterol accumulation and pigment formation of radish seedlings (Raphanus sativus L. cv. Saxa Treib) and in part also wheat seedlings (Triticum aestivum L. cv. Kolibri). Mevinolin applied during germination inhibits root elongation and development of lateral roots in etiolated and light‐grown radish seedlings. This effect cannot be overcome by exogenous GA3, but by addition of mevalonic acid, the product of the internally inhibited reaction. This emphazises the specifity of the mevinolin effect and indicates that the biosynthesis of mevalonic acid is a mandatory requirement for root growth. In light‐grown radish seedlings mevinolin also affects hypocotyl length‐growth and inhibits sterol accumulation, but has little effect on the chlorophyll and carotenoid accumulation in the chloroplasts of the cotyledons. This indicates the possible presence of an independent mevalonate synthesizing pathway within the plastids and suggests a low transport rate of mevinolin from the radish roots to the cotyledons. When mevinolin is directly applied to the leaves at higher concentrations, it also reduces the light‐induced chlorophyll and carotenoid accumulation as has been shown with etiolated primary leaves of wheat. This inhibition is age‐dependent and proceeds to a higher extent in older than in younger etiolated leaf tissue. From our results we conclude that plastids possess an independent HMG‐CoA reductase.In the cotyledons of radish, mevinolin seems to induce a senescence retardation and sun‐type growth response, as has been evaluated by measuring the fast and slow chlorophyll fluorescence induction kinetics (Kautsky effect). These responses may be due to inhibitor‐induced changes in the intracellular phytohormone balance.

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