The Biosynthesis of Feruloylated Compounds in Arabidopsis thaliana and Their Role in Development
Ferulic acid is found in the cell walls of most plant species where it cross-links cell wall polymers and may nucleate lignin polymerization. A substantial portion of ferulic acid, at least in Arabidopsis, is derived from the oxidation of the phenylpropanoid intermediate, coniferaldehyde, in a reaction catalyzed by a hydroxycinnamaldehyde dehydrogenase. The ccr1 mutant, which is defective in the gene encoding cinnamoyl CoA reductase (CCR1) an enzyme required for coniferaldehyde biosynthesis, is dwarf and accumulates feruloylated compounds not abundant in wild-type plants. The accumulation of these compounds in ccr1 suggests that they can be derived from an intermediate upstream of CCR1, such as feruloyl CoA, via a coniferaldehyde-independent pathway. In experiments aimed at defining the biosynthetic route of soluble feruloylated compounds in the ccr1 mutant, we crossed it to mutants defective in sinapic acid: UDP-glucose sinapoyltransferase (SGT), known as bright trichomes 1 (brt1), and sinapoylglucose: malate sinapoyltransferase (SMT), known as sinapoylglucose accumulator 1 (sng1), two enzymes involved in soluble hydroxycinnamoyl ester biosynthesis. Perhaps not unexpectedly, we observed that feruloylated compounds in the ccr1 mutant are dependent on both BRT1 and SMT which is consistent with the known pathway for sinapate ester biosynthesis in Arabidopsis. In contrast, we made the surprising observation that the brt1-1 ccr1 double mutant is sterile and more dwarf than ccr1 and that the ccr1 sng1-1 double mutant displays a wild-type growth phenotype. It has been suggested that the dwarf phenotype of ccr1 arises from the decreased lignin content which renders the vasculature insufficiently rigid for water transport which is required for proper growth and development. Neither BRT1 nor SMT are known to be involved in monolignol biosynthesis and thus it is puzzling that the sng1-1 mutation rescues the dwarf growth phenotype of ccr1 mutants and that the brt1-1 mutation exacerbates it. Other null alleles of SMT, known as sng1-5 and sng1-6, fail to rescue the dwarf growth phenotype of ccr1. In addition to being null for SMT, both sng1-5 and sng1-6 are null for sinapoylglucose: anthocyanin sinapoyltransferase (SAT). Therefore, SAT may be required for the rescued growth phenotype of ccr1 sng1-1 double mutants. These observations suggest that other phenylpropanoid metabolites, outside of monolignols, may directly impact the growth of plants through previously unidentified direct or indirect roles which may influence lignin biosynthesis.
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- Purdue University Department of Biochemistry Annual Retreat, Indiana (2012)