Prenylated proteins are required for methyl-jasmonate-induced monoterpenoid indole alkaloids biosynthesis in catharanthus roseus

Abstract

In Catharanthus roseus, monoterpenoid indole alkaloids (MIA) result from the condensation of the indole precursor tryptamine with the terpenoid precursor secologanin, which is derived from the plastidial methyl-d-erythritol 4-phosphate (MEP) pathway. Nevertheless, inhibition of the classical so-called mevalonate pathway leads to inhibition of MIA biosynthesis, suggesting that there is some cross regulation between these two pathways. The purpose of this chapter is to outline a new function for protein prenylation. Our results suggest that prenylated proteins, apparently mevalonate pathway end products, act as part of the regulatory mechanism coordinating the exchange of metabolites between compartmentalized metabolic pathways and that this process is governed by methyl jasmonate. Methyl jasmonate is a major inducer of alkaloid biosynthesis through enhancing MEP pathway gene expression. In C. roseus cells, inhibition of protein prenylation leads to the down-regulation of methyl-jasmonate-induced expression of MEP pathway genes and thus abolishes MIA biosynthesis. Jointly, failure of protein prenylation also inhibits the methyl-jasmonate-induced expression of the transcription factor ORCA3 which acts as a central regulator of MIA biosynthesis. Furthermore, the specific silencing of protein prenyltransferases in C. roseus cells mediated by RNA interference shows that inhibition of type I protein geranylgeranyltransferase down-regulates the expression of ORCA3. These data point to a specific role of protein geranylgeranylation in jasmonate signalling leading to MIA formation.