Summary The functions of phenylpropanoid compounds in plant defence range from preformed or inducible physical and chemical barriers against infection to signal molecules involved in local and systemic signalling for defence gene induction. Defensive functions are not restricted to a particular class of phenylpropanoid compound, but are found in the simple hydroxycinnamic acids and monolignols through to the more complex flavonoids, isoflavonoids, and stilbenes. The enzymatic steps involved in the biosynthesis of the major classes of phenylpropanoid compounds are now well established, and many of the corresponding genes have been cloned. Less is understood about the regulatory genes that orchestrate rapid, coordinated induction of phenylpropanoid defences in response to microbial attack. Many of the biosynthetic pathway enzymes are encoded by gene families, but the specific functions of individual family members remain to be determined. The availability of the complete genome sequence of Arabidopsis thaliana, and the extensive expressed sequence tag (EST) resources in other species, such as rice, soybean, barrel medic, and tomato, allow, for the first time, a full appreciation of the comparative genetic complexity of the phenylpropanoid pathway across species. In addition, gene expression array analysis and metabolic profiling approaches make possible comparative parallel analyses of global changes at the genome and metabolome levels, facilitating an understanding of the relationships between changes in specific transcripts and subsequent alterations in metabolism in response to infection.

Flavonoids are synthesized through an important metabolic pathway that leads to the production of diverse secondary metabolites, including anthocyanins, flavonols, flavones, and proanthocyanidins. Anthocyanins and flavonols are derived from Phe and share common precursors, dihydroflavonols, which are substrates for both flavonol synthase and dihydroflavonol 4-reductase. In the stems of Arabidopsis thaliana, anthocyanins accumulate in an acropetal manner, with the highest level at the junction between rosette and stem. We show here that this accumulation pattern is under the regulation of miR156-targeted SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) genes, which are deeply conserved and known to have important roles in regulating phase change and flowering. Increased miR156 activity promotes accumulation of anthocyanins, whereas reduced miR156 activity results in high levels of flavonols. We further provide evidence that at least one of the miR156 targets, SPL9, negatively regulates anthocyanin accumulation by directly preventing expression of anthocyanin biosynthetic genes through destabilization of a MYB-bHLH-WD40 transcriptional activation complex. Our results reveal a direct link between the transition to flowering and secondary metabolism and provide a potential target for manipulation of anthocyanin and flavonol content in plants.

Carbon nanodots (CDs) with a low cytotoxicity have been synthesized by one-step microwave-assisted pyrolysis of citric acid in the presence of various amine molecules. The primary amine molecules have been confirmed to serve dual roles as N-doping precursors and surface passivation agents, both of which considerably enhanced the fluorescence of the CDs.

Methanol synthesis from CO2 hydrogenation on the defective In2O3(110) surface with surface oxygen vacancies has been investigated using periodic density functional theory calculations. The relative stabilities of six possible surface oxygen vacancies numbered from Ov1 to Ov6 on the perfect In2O3(110) surface were examined. The calculated oxygen vacancy formation energies show that the D1 surface with the Ov1 defective site is the most thermodynamically favorable while the D4 surface with the Ov4 defective site is the least stable. Two different methanol synthesis routes from CO2 hydrogenation over both D1 and D4 surfaces were studied, and the D4 surface was found to be more favorable for CO2 activation and hydrogenation. On the D4 surface, one of the O atoms of the CO2 molecule fills in the Ov4 site upon adsorption. Hydrogenation of CO2 to HCOO on the D4 surface is both thermodynamically and kinetically favorable. Further hydrogenation of HCOO involves both forming the C–H bond and breaking the C–O bond, resulting in H2CO and hydroxyl. The HCOO hydrogenation is slightly endothermic with an activation barrier of 0.57 eV. A high barrier of 1.14 eV for the hydrogenation of H2CO to H3CO indicates that this step is the rate-limiting step in the methanol synthesis on the defective In2O3(110) surface.