Optical multistability in an optical ring cavity filled with a collection of three-level Lambda-type rubidium atoms has been experimentally demonstrated. The observed multistability is very sensitive to the induced atomic coherence in the system and can evolve from a normal bistable behavior with the change of the coupling field as well as the atomic number density. The underlying mechanism for the formation of such multistability is also discussed.

Reactive oxygen species (ROS) are transient, highly reactive intermediates or byproducts produced during oxygen metabolism. However, when innate mechanisms are unable to cope with sequestration of surplus ROS, it causes oxidative stress, where excess ROS damage biomolecules. Oxidized phosphatidylserine (PS), a pro-apoptotic “eat me” signal, is produced in response to elevated ROS, yet, little is known of its chemical composition and metabolism. Here, we report a small molecule that generates ROS in different mammalian cells, using which we detect, characterize and study oxidized PS in mammalian cells. We describe a chemical genetic screen to identify enzymes that regulate oxidized PS in mammalian cells, and find that the lipase ABHD12 hydrolyzes oxidized PS. We validate these findings in different physiological settings including primary peritoneal macrophages, and brains from Abhd12–/– knockout mice under inflammatory stress, and in the process functionally annotate an enzyme capable of regulating oxidized PS in vivo.

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Triglyceride-rich lipid droplets (LDs) are catabolized with high efficiency in hepatocytes to supply fatty acids for producing lipoprotein particles. Fasting causes a massive influx of adipose-derived fatty acids into the liver. The liver in the fasted state is therefore bloated with LDs but, remarkably, still continues to secrete triglycerides at a constant rate. Here we show that insulin signaling elevates phosphatidic acid (PA) dramatically on LDs in the fed state. PA then signals to recruit kinesin-1 motors, which transport LDs to the peripherally located smooth ER inside hepatocytes, where LDs are catabolized to produce lipoproteins. This pathway is down-regulated homeostatically when fasting causes insulin levels to drop, thus preventing dangerous elevation of triglycerides in the blood. Further, we show that a specific peptide against kinesin-1 blocks triglyceride secretion without any apparent deleterious effects on cells. Our work therefore reveals fundamental mechanisms that maintain lipid homeostasis across metabolic states and leverages this knowledge to propose a molecular target against hyperlipidemia.

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