57 research outputs found

    What lies beneath? Reconstructing the primitive magmas fueling voluminous silicic volcanism using olivine-hosted melt inclusions

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    Understanding the origins of the mantle melts that drive voluminous silicic volcanism is challenging because primitive magmas are generally trapped at depth. The central Taupō Volcanic Zone (TVZ; New Zealand) hosts an extraordinarily productive region of rhyolitic caldera volcanism. Accompanying and interspersed with the rhyolitic products, there are traces of basalt to andesite preserved as enclaves or pyroclasts in caldera eruption products and occurring as small monogenetic eruptive centers between calderas. These mafic materials contain MgO-rich olivines (Fo79–86) that host melt inclusions capturing the most primitive basaltic melts fueling the central TVZ. Olivine-hosted melt inclusion compositions associated with the caldera volcanoes (intracaldera samples) contrast with those from the nearby, mafic intercaldera monogenetic centers. Intracaldera melt inclusions from the modern caldera volcanoes of Taupō and Okataina have lower abundances of incompatible elements, reflecting distinct mantle melts. There is a direct link showing that caldera-related silicic volcanism is fueled by basaltic magmas that have resulted from higher degrees of partial melting of a more depleted mantle source, along with distinct subduction signatures. The locations and vigor of Taupō and Okataina are fundamentally related to the degree of melting and flux of basalt from the mantle, and intercaldera mafic eruptive products are thus not representative of the feeder magmas for the caldera volcanoes. Inherited olivines and their melt inclusions provide a unique “window” into the mantle dynamics that drive the active TVZ silicic magmatic systems and may present a useful approach at other volcanoes that show evidence for mafic recharge

    L-band Integral Field Spectroscopy of the HR 8799 Planetary System

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    Understanding the physical processes sculpting the appearance of young gas-giant planets is complicated by degeneracies confounding effective temperature, surface gravity, cloudiness, and chemistry. To enable more detailed studies, spectroscopic observations covering a wide range of wavelengths is required. Here we present the first L-band spectroscopic observations of HR 8799 d and e and the first low-resolution wide bandwidth L-band spectroscopic measurements of HR 8799 c. These measurements were facilitated by an upgraded LMIRCam/ALES instrument at the LBT, together with a new apodizing phase plate coronagraph. Our data are generally consistent with previous photometric observations covering similar wavelengths, yet there exists some tension with narrowband photometry for HR 8799 c. With the addition of our spectra, each of the three innermost observed planets in the HR 8799 system have had their spectral energy distributions measured with integral field spectroscopy covering 0.9\sim0.9 to 4.1 μm4.1~\mu\mathrm{m}. We combine these spectra with measurements from the literature and fit synthetic model atmospheres. We demonstrate that the bolometric luminosity of the planets is not sensitive to the choice of model atmosphere used to interpolate between measurements and extrapolate beyond them. Combining luminosity with age and mass constraints, we show that the predictions of evolutionary models are narrowly peaked for effective temperature, surface gravity, and planetary radius. By holding these parameters at their predicted values, we show that more flexible cloud models can provide good fits to the data while being consistent with the expectations of evolutionary models.Comment: 19 pages, 11 figures, accepted for publication in The Astronomical Journal; added reference, updated figure 6 and table

    Mechanisms Underlying the Confined Diffusion of Cholera Toxin B-Subunit in Intact Cell Membranes

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    Multivalent glycolipid binding toxins such as cholera toxin have the capacity to cluster glycolipids, a process thought to be important for their functional uptake into cells. In contrast to the highly dynamic properties of lipid probes and many lipid-anchored proteins, the B-subunit of cholera toxin (CTxB) diffuses extremely slowly when bound to its glycolipid receptor GM1 in the plasma membrane of living cells. In the current study, we used confocal FRAP to examine the origins of this slow diffusion of the CTxB/GM1 complex at the cell surface, relative to the behavior of a representative GPI-anchored protein, transmembrane protein, and fluorescent lipid analog. We show that the diffusion of CTxB is impeded by actin- and ATP-dependent processes, but is unaffected by caveolae. At physiological temperature, the diffusion of several cell surface markers is unchanged in the presence of CTxB, suggesting that binding of CTxB to membranes does not alter the organization of the plasma membrane in a way that influences the diffusion of other molecules. Furthermore, diffusion of the B-subunit of another glycolipid-binding toxin, Shiga toxin, is significantly faster than that of CTxB, indicating that the confined diffusion of CTxB is not a simple function of its ability to cluster glycolipids. By identifying underlying mechanisms that control CTxB dynamics at the cell surface, these findings help to delineate the fundamental properties of toxin-receptor complexes in intact cell membranes

    Stage-Specific Pathways of Leishmania infantum chagasi Entry and Phagosome Maturation in Macrophages

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    The life stages of Leishmania spp. include the infectious promastigote and the replicative intracellular amastigote. Each stage is phagocytosed by macrophages during the parasite life cycle. We previously showed that caveolae, a subset of cholesterol-rich membrane lipid rafts, facilitate uptake and intracellular survival of virulent promastigotes by macrophages, at least in part, by delaying parasitophorous vacuole (PV)-lysosome fusion. We hypothesized that amastigotes and promastigotes would differ in their route of macrophage entry and mechanism of PV maturation. Indeed, transient disruption of macrophage lipid rafts decreased the entry of promastigotes, but not amastigotes, into macrophages (P<0.001). Promastigote-containing PVs were positive for caveolin-1, and co-localized transiently with EEA-1 and Rab5 at 5 minutes. Amastigote-generated PVs lacked caveolin-1 but retained Rab5 and EEA-1 for at least 30 minutes or 2 hours, respectively. Coinciding with their conversion into amastigotes, the number of promastigote PVs positive for LAMP-1 increased from 20% at 1 hour, to 46% by 24 hours, (P<0.001, Chi square). In contrast, more than 80% of amastigote-initiated PVs were LAMP-1+ at both 1 and 24 hours. Furthermore, lipid raft disruption increased LAMP-1 recruitment to promastigote, but not to amastigote-containing compartments. Overall, our data showed that promastigotes enter macrophages through cholesterol-rich domains like caveolae to delay fusion with lysosomes. In contrast, amastigotes enter through a non-caveolae pathway, and their PVs rapidly fuse with late endosomes but prolong their association with early endosome markers. These results suggest a model in which promastigotes and amastigotes use different mechanisms to enter macrophages, modulate the kinetics of phagosome maturation, and facilitate their intracellular survival
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