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Two Japanese scientists supply hundreds of laboratories with a prized gem — and are now among the world’s most published researchers. Two Japanese scientists supply hundreds of laboratories with a prized gem — and are now among the world’s most published researchers. Takashi Taniguchi prepares the 30,000 ton press to make a new batch of hexagonal boron nitride crystals.

The deadly virus is one of five that have been brought to a secure laboratory. The deadly virus is one of five that have been brought to a secure laboratory.

Low-cost hobbyist machines print by squeezing out thin plastic filaments from heated nozzles, building up a structure layer by layer - a method known as fused deposition modelling (FDM). [...]last January, Scott and his colleague Mark Burns at the University of Michigan in Ann Arbor reported a printer that inhibits the reactions by mixing into the resin a chemical that can be activated by a second lamp emitting a different wavelength of light4. The approach has garnered substantial interest from industry, says Christopher Spadaccini, a materials and manufacturing engineer at Lawrence Livermore National Laboratory (LLNL) in California. [...]really, what you need is a halfway-decent projector and a rotating stage,\" he says. First displayed publicly in 2018, the bridge is now being tested and having sensors installed ahead of a planned

A 2018 study1 of satellite data from the US National Oceanic and Atmospheric Administration found that forest cover has increased in line with government statistics, but suggested that changes in logging policy were more important than afforestation - planting forests where none were before. A paper2 co-authored by Sternberg found that arid areas in China had increased by roughly 1.6 million square kilometres, about the size of Iran, since 1980 - probably due largely to anthropogenic climate change. A 2016 study3 found that the revitalized ecosystem is already sucking up rainfall and reducing the amount of water that runs off to rivers; a drier climate could exacerbate the situation and trigger water shortages for humans.

Genetically encoded dopamine sensors based on green fluorescent protein (GFP) enable high-resolution imaging of dopamine dynamics in behaving animals. However, these GFP-based variants cannot be readily combined with commonly used optical sensors and actuators, due to spectral overlap. We therefore engineered red-shifted variants of dopamine sensors called RdLight1, based on mApple. RdLight1 can be combined with GFP-based sensors with minimal interference and shows high photostability, permitting prolonged continuous imaging. We demonstrate the utility of RdLight1 for receptor-specific pharmacological analysis in cell culture, simultaneous assessment of dopamine release and cell-type-specific neuronal activity and simultaneous subsecond monitoring of multiple neurotransmitters in freely behaving rats. Dual-color photometry revealed that dopamine release in the nucleus accumbens evoked by reward-predictive cues is accompanied by a rapid suppression of glutamate release. By enabling multiplexed imaging of dopamine with other circuit components in vivo, RdLight1 opens avenues for understanding many aspects of dopamine biology. Red and yellow versions of the genetically encoded dopamine sensor dLight1 have been developed and allow multiplexed imaging of dopamine with neurotransmitter or cell-type-specific calcium combined with green sensors or actuators, as demonstrated ex vivo and in behaving rodents.

Researchers warn that the country’s push to hold back its deserts could strain water resources. Researchers warn that the country’s push to hold back its deserts could strain water resources. The view of planted trees in desert are seen from an aircraft on March 28th, 2019 in Wuwei, Gansu Province. Credit: Wang He/Getty

Neuromodulator release alters the function of target circuits in poorly known ways. An essential step to address this knowledge gap is to measure the dynamics of neuromodulatory signals while simultaneously manipulating the elements of the target circuit during behavior. Patriarchi et al. developed fluorescent protein–based dopamine indicators to visualize spatial and temporal release of dopamine directly with high fidelity and resolution. In the cortex, two-photon imaging with these indicators was used to map dopamine activity at cellular resolution. Science , this issue p. eaat4422 Genetically encoded indicators allow optical measurement of dopamine release in vivo at high spatiotemporal resolution. Neuromodulatory systems exert profound influences on brain function. Understanding how these systems modify the operating mode of target circuits requires spatiotemporally precise measurement of neuromodulator release. We developed dLight1, an intensity-based genetically encoded dopamine indicator, to enable optical recording of dopamine dynamics with high spatiotemporal resolution in behaving mice. We demonstrated the utility of dLight1 by imaging dopamine dynamics simultaneously with pharmacological manipulation, electrophysiological or optogenetic stimulation, and calcium imaging of local neuronal activity. dLight1 enabled chronic tracking of learning-induced changes in millisecond dopamine transients in mouse striatum. Further, we used dLight1 to image spatially distinct, functionally heterogeneous dopamine transients relevant to learning and motor control in mouse cortex. We also validated our sensor design platform for developing norepinephrine, serotonin, melatonin, and opioid neuropeptide indicators.

β-Arrestins are master regulators of cellular signaling that operate by desensitizing ligand-activated G-protein-coupled receptors (GPCRs) at the plasma membrane and promoting their subsequent endocytosis. The endocytic activity of β-arrestins is ligand dependent, triggered by GPCR binding, and increasingly recognized to have a multitude of downstream signaling and trafficking consequences that are specifically programmed by the bound GPCR. However, only one biochemical ‘mode’ for GPCR-mediated triggering of the endocytic activity is presently known – displacement of the β-arrestin C-terminus (CT) to expose clathrin-coated pit-binding determinants that are masked in the inactive state. Here, we revise this view by uncovering a second mode of GPCR-triggered endocytic activity that is independent of the β-arrestin CT and, instead, requires the cytosolic base of the β-arrestin C-lobe (CLB). We further show each of the discrete endocytic modes is triggered in a receptor-specific manner, with GPCRs that bind β-arrestin transiently (‘class A’) primarily triggering the CLB-dependent mode and GPCRs that bind more stably (‘class B’) triggering both the CT and CLB-dependent modes in combination. Moreover, we show that different modes have opposing effects on the net signaling output of receptors – with the CLB-dependent mode promoting rapid signal desensitization and the CT-dependent mode enabling prolonged signaling. Together, these results fundamentally revise understanding of how β-arrestins operate as efficient endocytic adaptors while facilitating diversity and flexibility in the control of cell signaling.

Most monogenic cases of obesity in humans have been linked to mutations in genes encoding members of the leptin–melanocortin pathway. Specifically, mutations in MC4R , the melanocortin-4 receptor gene, account for 3–5% of all severe obesity cases in humans 1 – 3 . Recently, ADCY3 (adenylyl cyclase 3) gene mutations have been implicated in obesity 4 , 5 . ADCY3 localizes to the primary cilia of neurons 6 , organelles that function as hubs for select signaling pathways. Mutations that disrupt the functions of primary cilia cause ciliopathies, rare recessive pleiotropic diseases in which obesity is a cardinal manifestation 7 . We demonstrate that MC4R colocalizes with ADCY3 at the primary cilia of a subset of hypothalamic neurons, that obesity-associated MC4R mutations impair ciliary localization and that inhibition of adenylyl cyclase signaling at the primary cilia of these neurons increases body weight. These data suggest that impaired signaling from the primary cilia of MC4R neurons is a common pathway underlying genetic causes of obesity in humans. MC4R colocalizes with ADCY3 at primary cilia in hypothalamic neurons, and MC4R mutations associated with human obesity impair this localization. Inhibition of adenylyl cyclase signaling at primary cilia of neurons leads to increased body weight in mice.