Fruit size: Towards an understanding of the metabolic control of fruit growth using avocado as a model system

Abstract

Final fruit size is the consequence of complex metabolic events that occur between fruit set and maturation. Disruption of these biochemical and molecular processes at any stage during fruit growth will impact on final fruit size. Because fruit size is a function of cell number rather than cell size, factors affecting cell division cycle activity assume importance. In this paper, we focus attention on the metabolic control of fruit growth using avocado as a model system. Three areas of current interest are highlighted, viz. the contribution by isoprenoid metabolism in the control of cell proliferation, the role played by carbohydrate content and composition in signalling changes in metabolite status and gene expression and maintenance of plant hormone homeostasis. Central to the process of fruit growth and control of final fruit size by cell division is 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase (HMGR) and activity of the sucrose non‐fermenting 1‐related protein kinase (SnRK1) complex. It is argued that sugar content and composition of sink cells impact on SnRK1 (and hexokinase) to modulate expression of sugar‐metabolizing enzymes, HMGR and molybdenum cofactor (MoCo)‐containing enzymes. These changes, in turn, impact on hormone metabolism by affecting allocation of the purine‐derived MoCo to aldehyde oxidase and thus the endogenous concentration of indole‐3‐acetic acid, abscisic acid and cytokinin (CK) to alter plant hormone homeostasis. These aspects are integrated into a model to explain the metabolic control of avocado fruit growth and final fruit size.