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e., are doubted less) than objective facts. These results provide a concrete demonstration of how to bridge moral divides while also revealing how our intuitions can lead us astray. Stretching back to the Enlightenment, philosophers and scientists have privileged objective facts over experiences in the pursuit of truth. However, furnishing perceptions of truth within moral disagreements is better accomplished by sharing subjective experiences, not by providing facts.The productivity of aquatic ecosystems depends on the supply of limiting nutrients. The invasion of the Laurentian Great Lakes, the world's largest freshwater ecosystem, by dreissenid (zebra and quagga) mussels has dramatically altered the ecology of these lakes. A key open question is how dreissenids affect the cycling of phosphorus (P), the nutrient that limits productivity in the Great Lakes. We show that a single species, the quagga mussel, is now the primary regulator of P cycling in the lower four Great Lakes. By virtue of their enormous biomass, quagga mussels sequester large quantities of P in their tissues and dramatically intensify benthic P exchanges. Mass balance analysis reveals a previously unrecognized sensitivity of the Great Lakes ecosystem, where P availability is now regulated by the dynamics of mussel populations while the role of the external inputs of phosphorus is suppressed. Our results show that a single invasive species can have dramatic consequences for geochemical cycles even in the world's largest aquatic ecosystems. The ongoing spread of dreissenids across a multitude of lakes in North America and Europe is likely to affect carbon and nutrient cycling in these systems for many decades, with important implications for water quality management.Epidemic preparedness depends on our ability to predict the trajectory of an epidemic and the human behavior that drives spread in the event of an outbreak. Changes to behavior during an outbreak limit the reliability of syndromic surveillance using large-scale data sources, such as online social media or search behavior, which could otherwise supplement healthcare-based outbreak-prediction methods. Here, we measure behavior change reflected in mobile-phone call-detail records (CDRs), a source of passively collected real-time behavioral information, using an anonymously linked dataset of cell-phone users and their date of influenza-like illness diagnosis during the 2009 H1N1v pandemic. We demonstrate that mobile-phone use during illness differs measurably from routine behavior Diagnosed individuals exhibit less movement than normal (1.1 to 1.4 fewer unique tower locations; [Formula see text]), on average, in the 2 to 4 d around diagnosis and place fewer calls (2.3 to 3.3 fewer calls; [Formula see text]) while spending longer on the phone (41- to 66-s average increase; [Formula see text]) than usual on the day following diagnosis. The results suggest that anonymously linked CDRs and health data may be sufficiently granular to augment epidemic surveillance efforts and that infectious disease-modeling efforts lacking explicit behavior-change mechanisms need to be revisited.Upon activation by different transmembrane receptors, the same signaling protein can induce distinct cellular responses. A way to decipher the mechanisms of such pleiotropic signaling activity is to directly manipulate the decision-making activity that supports the selection between distinct cellular responses. We developed an optogenetic probe (optoSRC) to control SRC signaling, an example of a pleiotropic signaling node, and we demonstrated its ability to generate different acto-adhesive structures (lamellipodia or invadosomes) upon distinct spatio-temporal control of SRC kinase activity. The occurrence of each acto-adhesive structure was simply dictated by the dynamics of optoSRC nanoclusters in adhesive sites, which were dependent on the SH3 and Unique domains of the protein. The different decision-making events regulated by optoSRC dynamics induced distinct downstream signaling pathways, which we characterized using time-resolved proteomic and network analyses. Collectively, by manipulating the molecular mobility of SRC kinase activity, these experiments reveal the pleiotropy-encoding mechanism of SRC signaling.Bidirectional transport of macromolecules across the nuclear envelope is a hallmark of eukaryotic cells, in which the genetic material is compartmentalized inside the nucleus. The nuclear pore complex (NPC) is the major gateway to the nucleus and it regulates nucleocytoplasmic transport, which is key to processes including transcriptional regulation and cell cycle control. Tanespimycin Accordingly, components of the nuclear transport machinery are often found to be dysregulated or hijacked in diseases. In this Cell Science at a Glance article and accompanying poster, we provide an overview of our current understanding of cargo transport through the NPC, from the basic transport signals and machinery to more emerging aspects, all from a 'cargo perspective'. Among these, we discuss the transport of large cargoes (>15 nm), as well as the roles of different cargo properties to nuclear transport, from size and number of bound nuclear transport receptors (NTRs), to surface and mechanical properties.The entorhinal cortex (EC) is a vital component of the medial temporal lobe, and its contributions to cognitive processes and memory formation are supported through its extensive interconnections with the hippocampal formation. During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurodegeneration in the EC and hippocampus during AD has been clearly linked to impairments in memory and cognitive function, and a growing body of evidence indicates that molecular and functional neurodegeneration within the EC may play a primary role in cognitive decline in the early phases of AD. Defining the mechanisms underlying molecular neurodegeneration in the EC is crucial to determining its contributions to the pathogenesis of AD. Surprisingly few studies have focused on understanding the mechanisms of molecular neurodegeneration and selective vulnerability within the EC. However, there have been advancements indicating that early dysregulation of cellular and molecular signaling pathways in the EC involve neurodegenerative cascades including oxidative stress, neuroinflammation, glia activation, stress kinases activation, and neuronal loss.