Abstract

There is considerable evidence that the rates of phytoalexin synthesis relative to those of secondary colonization by pathogens is a critical determinant of disease resistance in most plants.1 For example, resistance of cotton cultivars to fungal wilt pathogens, the bacterial blight pathogen, and nematodes is directly related to how rapidly terpenoid phytoalexins accumulate in infected tissues.2 HMGR (3-hydroxy-3-methylglutaryl-CoA reductase) is one of the first enzymes in the terpenoid pathway and often plays a regulatory role for biosynthesis of steroids and terpenoids in plants and animals. Increases in activity of HMGR and accumulation of mRNA for HMGR slightly precede and occur parallel to the accumulation of terpenoid phytoalexins in cotton cultivars infected with Verticillium dahliae.3,4 Genetic manipulation of the HMGR genes or regulatory genes affecting them to give more rapid synthesis of phytoalexins is one approach for improving disease resistance in cotton and other plant species that have terpenoid phytoalexins.

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