The structural homogeneity and acid stability of linear C-lignins allow their deconstruction to useful monomers in high yield.

Metal halide perovskite nanocrystals (NCs) are attractive materials for optoelectronics. However, further improvements in stability, reproducibility, and photoluminescence quantum yield (Φ PL ) are essential for enabling future applications. Inadequate surface passivation is a major cause of instability, irreproducibility, and less than unity Φ PL . Herein, we probe the influence of multiple ligand binding groups on the colloidal stability and Φ PL of CsPbBr 3 nanocrystals (NCs). We find that post-synthetic treatment with dodecanethiol reproducibly yields highly stable NCs with near-unity Φ PL for a range of synthetic conditions and initial Φ PL of the as-synthesized NCs. A mechanistic investigation shows that thiol addition leads to thioether formation via the thiol−ene reaction with octadecene, oleic acid, and oleylamine. Both thiolates and thioethers are suspected to bind to undercoordinated Pb atoms on the NC surfaces, and this surface binding can be rapidly accelerated through exposure to blue or UV light. Furthermore, we show that metallic Pb nanoparticles appear in many batches of synthesized CsPbBr 3 NCs and that dodecanethiol addition eliminates these metallic Pb particles.

X-ray crystal structures of a phenothiazine posolyte and viologen negolyte and cyclic voltammograms of a solution containing both compounds.

The plant cuticle is often considered a passive barrier from the environment. We show that the cuticle regulates active transport of the defense hormone salicylic acid (SA). SA, an important regulator of systemic acquired resistance (SAR), is preferentially transported from pathogen-infected to uninfected parts via the apoplast. Apoplastic accumulation of SA, which precedes its accumulation in the cytosol, is driven by the pH gradient and deprotonation of SA. In cuticle-defective mutants, increased transpiration and reduced water potential preferentially routes SA to cuticle wax rather than to the apoplast. This results in defective long-distance transport of SA, which in turn impairs distal accumulation of the SAR-inducer pipecolic acid. High humidity reduces transpiration to restore systemic SA transport and, thereby, SAR in cuticle-defective mutants. Together, our results demonstrate that long-distance mobility of SA is essential for SAR and that partitioning of SA between the symplast and cuticle is regulated by transpiration.