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Genetic Tango of Sleep-Wake Rhythms Spins on a New Adaptor

Scientists at Northwestern University have demonstrated that the loss of a gene called Tango10 affects daily behavior in fruit flies and disrupts their 24-hour sleep-wake cycles. The protein’s expression in pacemaker neurons regulates their neuronal activity, potentially through voltage-gated potassium channel currents, that in turn regulate circadian behavior in flies. Since Tango10 is a conserved protein, the study could help identify and treat analogous defects in humans with clock-related disorders.

Alzheimer’s Disease Pathology Curbed Using Aromatic Compound in Basil

New research shows a natural compound in basil called fenchol may protect against Alzheimer’s disease pathology. A University of South Florida Health-led team discovered that the aromatic compound fenchol has the same beneficial effect as gut-derived short chain fatty acid (SCFA) metabolites in reducing neurotoxic amyloid-beta in the brain. The authors reported that fenchol, like SCFAs, activates fatty acid receptor 2 (FFAR2) on neurons in the brain, increasing lysosomal and proteasomal activity and decreasing amyloid beta-induced neurotoxicity and neuronal cell death.

Allergies? Blame the Ripoptosome, an Allergen-Sensing “Platform”

Researchers at the Cincinnati Children’s Hospital Medical Center have identified a novel pathway they call the RIPIL-33 pathway that assembles in many types of epithelial cells upon exposure to various unrelated environmental allergens and processes the cytokine IL-33 into an active form within the cell to aid cellular recognition of the allergens. The new rapid reaction system may hold the key to understanding and treating people suffering from a wide range of allergies.

Shigella Enzyme Blocks Human Cell Death to Establish Infection

Research from Genentech and the University of California has improved upon the sole animal model of shigella infection, providing an indispensable tool for vaccine development. The study identifies the mechanism Shigella adopts to prevent programmed cell death of the infected host intestinal cells and enable infection. IpaH7.8, a Shigella ubiquitin ligase, inhibits a host pore-forming protein (GSDMD) that induces cell death. Eliminating GSDMD in mice already primed for Shigella infection, increases bacterial replication and disease severity, generating an improved model for human Shigellosis.