Benzoxazinoids are important defense compounds in grasses. Here, we investigated the biosynthesis and biological roles of the 8-O-methylated benzoxazinoids, DIM 2 BOA-Glc and HDM 2 BOA-Glc. Using quantitative trait locus mapping and heterologous expression, we identified a 2-oxoglutarate-dependent dioxygenase (BX13) that catalyzes the conversion of DIMBOA-Glc into a new benzoxazinoid intermediate (TRIMBOA-Glc) by an uncommon reaction involving a hydroxylation and a likely ortho-rearrangement of a methoxy group. TRIMBOA-Glc is then converted to DIM 2 BOA-Glc by a previously described O-methyltransferase BX7. Furthermore, we identified an O-methyltransferase (BX14) that converts DIM 2 BOA-Glc to HDM 2 BOA-Glc. The role of these enzymes in vivo was demonstrated by characterizing recombinant inbred lines, including Oh43, which has a point mutation in the start codon of Bx13 and lacks both DIM 2 BOA-Glc and HDM 2 BOA-Glc, and Il14H, which has an inactive Bx14 allele and lacks HDM 2 BOA-Glc in leaves. Experiments with near-isogenic maize lines derived from crosses between B73 and Oh43 revealed that the absence of DIM 2 BOA-Glc and HDM 2 BOA-Glc does not alter the constitutive accumulation or deglucosylation of other benzoxazinoids. The growth of various chewing herbivores was not significantly affected by the absence of BX13-dependent metabolites, while aphid performance increased, suggesting that DIM 2 BOA-Glc and/or HDM 2 BOA-Glc provide specific protection against phloem feeding insects.
The defense of plants against herbivores and pathogens involves the participation of an enormous range of different metabolites, some of which act directly as defensive weapons against enemies (toxins or deterrents) and some of which act as components of the complex internal signaling network that insures that defense is timed to enemy attack. Recent work reveals a surprising trend: The same compounds may act as both weapons and signals of defense. For example, two groups of well-studied defensive weapons, glucosinolates and benzoxazinoids, trigger the accumulation of the protective polysaccharide callose as a barrier against aphids and pathogens. In the other direction, several hormones acting in defense signaling (and their precursors and products) exhibit activity as weapons against pathogens. Knowing which compounds are defensive weapons, which are defensive signals and which are both is vital for understanding the functioning of plant defense systems.
The induced production of secondary metabolites in herbivore-attacked plants varies in space and time. However, the consequences of these spatiotemporal patterns for herbivore performance are not well understood. This is particularly true for 1,4-benzoxazin-3-ones (BXs), the major induced defensive metabolites of maize. Here we report on the spatiotemporal dynamics of BX induction and its consequences for the leaf feeder Spodoptera littoralis. Defence-related phytohormones and transcript levels of BX biosynthetic genes were upregulated locally at the wound site within 12 h of herbivory. Within another 12 h, the insecticidal BX HDMBOA-Glc started to accumulate in a highly localized manner at the feeding site. Changes in BX metabolism away from the feeding site within the same leaf were much weaker and were undetected in systemic leaves. Following the removal of the caterpillars, local HDMBOA-Glc levels remained elevated for 7 days. Caterpillars that were forced to feed directly on locally induced leaf parts, but not on adjacent leaf parts, suffered from reduced growth. This effect was abolished in the BX-deficient bx1 mutant. We did not find any evidence that BXs regulate defensive phytohormones or their own accumulation. In summary, this study shows that induced herbivore resistance in maize is highly localized and dependent on BXs.
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