INFECTIOUS DISEASE
▸ Inflammation encourages spread of bacterial viruses
CREDIT: IND. ENG. CHEM. RES. (NAIL POLISH); THOMAS C. BOOTHBY/UNC CHAPEL HILL (WATER BEARS)
Downloaded via UNIV OF SOUTH DAKOTA on July 20, 2018 at 17:45:02 (UTC). See https://pubs.acs.org/sharingguidelines for options on how to legitimately share published articles.
done (Angew. Chem. Int. Ed. 2017, DOI: 10.1002/anie.201611851). The researchers previously created several main-group complexes containing Si=O, O–Si=O, or O=Si-OH units supported by electron-donating and/or electron-accepting ligands. Ultimately they found that pairing an amine-substituted pyridine donor ligand and an iminophosphorane-based donor-acceptor ligand creates a stable environment for SiO2. The new complex is soluble in organic solvents and is a stable solid at room temperature. But most interesting, the researchers say, is that the complex can be used as an SiO2-transfer reagent. In an initial test, they show that the complex reacts with phenylsilane to produce a trisiloxane. The team is continuing to explore the reaction chemistry of the new complex, including its ability to produce chiral SiO2-containing molecules.—STEVE RITTER
Pathogenic bacteria sometimes wreak havoc thanks to viral invaders called bacteriophages. Some phages infect bacteria and incorporate their DNA, as well as genes for toxins and other virulence factors, into the genomes of the microbes. In fact, the genes for the cholera toxin came from a phage that infected the ancestor of Vibrio cholerae. Such phages lie dormant and then reawaken and burst out of bacteria to infect other bacteria nearby, spreading the virulence genes they carry in the process. A new study reports that inflammation caused when the immune system attacks bacteria triggers this viral spread between microbes (Science 2017, DOI: 10.1126/science.aaf8451). The findings suggest that vaccinations and other treatments that avoid inflammation could slow the evolution of pathogens. The researchers led by Médéric Diard and Wolf-Dietrich Hardt of ETH Zurich studied mice infected with two strains of Salmonella enterica Typhimurium: a donor that contained a phage and a recipient that did not. After three days in the mice, 58% of the recipient microbes had been infected by the phage. But when the team used Salmonella engineered to not trigger inflammation, less than 0.01% of the recipient microbes carried the phage. Also, when the team infected mice vaccinated against Salmonella, the researchers observed less gut inflam-
NANOMATERIALS
‘Goldfinger’ nails Marcus Lau found inspiration lodged somewhere in the 50-odd bottles of nail polish in his fiancé’s bathroom drawers. “I soon realized that one thing was always missing: a real gold-containing polish,” he says, now happily married. It occurred to Lau that he could use the laser in the lab at the University of Duisburg-Essen, where he is a postdoc, to create a cosmetic out of gold nanoparticles. Working with his mentor Stephan Barcikowski and graduate student Friedrich Waag, Lau developed a method to directly integrate metal nanoparticles into nail polish (Ind. Eng. Chem. Res. 2017, DOI: 10.1021/acs. iecr.7b00039). The researchers placed Nanoparticle nail polishes (from left): none, a metal plate—gold, platinum, silver, gold-silver alloy, and gold. silver, platinum, or a gold-silver alloy—into a glass vessel and covered it with clear, colorless nail polish. They then used laser ablation to zap metal nanoparticles into the polish over the course of 15 minutes. The nanoparticles have no corona of residual chemicals or capping agents, Barcikowski points out, which are tricks typically used to get nanoparticles into viscous liquids. In addition to creating metallic nail polishes, the chemists note that the coatings could be used for biomedical applications. The nanoparticles in the silver polish, specifically, appear to break down into silver ions, which have antibacterial properties.—BETHANY HALFORD
mation and, as a result, less phage transfer.—MICHAEL TORRICE
BIOLOGICAL CHEMISTRY
that the slowly dried creatures expressed genes for several families of IDPs, which lack well-defined tertiary structure, and that this gene expression is required to sur-
▸ Water bears deploy disordered proteins to survive desiccation Tardigrades, known affectionately as water bears, are microscopic, eight-legged creatures renowned for their ability to live through extreme environmental stresses, including desiccation, freezing, high pressure, radiation exposure, and even the vacuum of space. Intrinsically disordered proteins (IDPs) may be the key to how tardigrades survive desiccation, according to a new study (Mol. Cell 2017, DOI: 10.1016/j. molcel.2017.02.018). A research team led by Thomas C. Boothby and Gary J. Pielak at the University of North Carolina, Chapel Hill, compared gene expression of hydrated and slowly dried tardigrades. They found
Several slowly dried tardigrades in their desiccated “tun” state. vive desiccation. The researchers expressed tardigrade IDP genes in bacteria and yeast and found that the proteins induced desiccation tolerance in those organisms as well. The researchers suggest that IDPs form an amorphous, glasslike matrix in the drying-out tardigrade cells that protects other proteins from denaturation and aggregation.—JYLLIAN KEMSLEY MARCH 20, 2017 | CEN.ACS.ORG | C&EN
9
