METABOLIC CONTROL OF AVOCADO FRUIT-GROWTH - ISOPRENOID GROWTH-REGULATORS AND THE REACTION CATALYZED BY 3-HYDROXY-3-METHYLGLUTARYL COENZYME-A REDUCTASE

The effect of isoprenoid growth regulators on avocado (Persea american a Mill. cv Hass) fruit growth and mesocarp 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity was investigated during the cours e of fruit ontogeny. Both normal and small-fruit phenotypes were used to probe the interaction between the end products of isoprenoid biosyn thesis and the activity of HMGR in the metabolic control of avocado fr uit growth. Kinetic analysis of the changes in both cell number and si ze revealed that growth was limited by cell number in phenotypically s mall fruit. In small fruit a 70% reduction in microsomal HMGR activity was associated with an increased mesocarp abscisic acid (ABA) concent ration. Application of mevastatin, a competitive inhibitor of HMGR, re duced the growth of normal fruit and increased mesocarp ABA concentrat ion. These effects were reversed by co-treatment of fruit with mevalon ic acid lactone, isopentenyladenine, or N-(2-chloro-4-pyridyl)-N-pheny lurea, but were not significantly affected by either gibberellic acid or stigmasterol. However, stigmasterol appeared to partially restore f ruit growth when co-injected with mevastatin in either phase It or III of fruit growth. In vivo application of ABA reduced fruit growth and mesocarp HMGR activity and accelerated fruit abscission, effects that were reversed by co-treatment with isopentenyladenine. Together, these observations indicate that ABA accumulation down-regulates mesocarp H MGR activity and fruit growth, and that in situ cytokinin biosynthesis modulates these effects during phase I of fruit ontogeny, whereas bot h cytokinins and sterols seem to perform this function during the late r phases.