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Abstract Spongy clinopyroxene is common in most mantle-derived xenoliths and megacrysts of eclogitic and peridotitic parageneses. Its formation is commonly attributed to the partial melting of a primary clinopyroxene in response to various factors, including changes in pressure and temperature or infiltration of external melts or fluids. In order to study the mechanism of spongy clinopyroxene formation in detail, we selected six eclogitic clinopyroxene inclusions in diamonds with varying amounts of spongy clinopyroxene (from ~10 to 100%). We employed computed tomography, electron microprobe analysis, and Raman spectroscopy to study the textural characteristics, major element concentrations, and the types of volatiles present in both phases. We also used pMELTS to model the compositions of spongy clinopyroxene and associated melts produced by the melting of primary clinopyroxene over a range of pressures and temperatures. We compare these results with estimates from major element thermobarometry of the spongy clinopyroxene. We conclude that the studied spongy clinopyroxene is the solid product of partial melting that occurs upon decompression of the primary clinopyroxene within the diamond in a near-closed system. Melting of the primary clinopyroxene occurred continuously or in pulses at different depths during the diamond’s ascent to Earth’s surface and produced variable spongy clinopyroxene and melt compositions even within the same inclusion. This is possible due to relatively rapid kimberlite ascent. The degrees of melting are various and unexpectedly high for mantle melting (between <10 and 60% with an average of ~20–30%). The produced melts are highly silicic, phonolitic, and alkali-rich. pMELTS modelling shows the spongy clinopyroxene compositions can be reproduced at pressures between 0.5–2.7 GPa and temperatures of 850–1300°C, with the majority of them satisfying the P–T conditions of 1–2 GPa and 1100–1300°C. This indicates decompression melting of primary clinopyroxene at shallow upper mantle or lower crustal conditions. 

ABSTRACT An increase in atmospheric pO2 has been proposed as a trigger for the Cambrian Explosion at ∼539–514 Ma but the mechanistic linkage remains unclear. To gain insights into marine habitability for the Cambrian Explosion, we analysed excess Ba contents (Baexcess) and isotope compositions (δ138Baexcess) of ∼521-Myr-old metalliferous black shales in South China. The δ138Baexcess values vary within a large range and show a negative logarithmic correlation with Baexcess, suggesting a major (>99%) drawdown of oceanic Ba inventory via barite precipitation. Spatial variations in Baexcess and δ138Baexcess indicate that Ba removal was driven by sulfate availability that was ultimately derived from the upwelling of deep seawaters. Global oceanic oxygenation across the Ediacaran–Cambrian transition may have increased the sulfate reservoir via oxidation of sulfide and concurrently decreased the Ba reservoir by barite precipitation. The removal of both H2S and Ba that are deleterious to animals could have improved marine habitability for early animals. 

Cell spreading and migration play central roles in many physiological and pathophysiological processes. We have previously shown that MFN2 regulates the migration of human neutrophil-like cells via suppressing Rac activation. Here, we show that in mouse embryonic fibroblasts, MFN2 suppresses RhoA activation and supports cell polarization. After initial spreading, the wild-type cells polarize and migrate, whereas theMfn2^-/-cells maintain a circular shape. Increased cytosolic Ca²⁺resulting from the loss of Mfn2 is directly responsible for this phenotype, which can be rescued by expressing an artificial tether to bring mitochondria and endoplasmic reticulum to close vicinity. Elevated cytosolic Ca²⁺activates Ca²⁺/calmodulin-dependent protein kinase II, RhoA, and myosin light-chain kinase, causing an overactivation of nonmuscle myosin II, leading to a formation of a prominent F-actin ring at the cell periphery and increased cell contractility. The peripheral actin band alters cell physics and is dependent on substrate rigidity. Our results provide a novel molecular basis to understand how MFN2 regulates distinct signaling pathways in different cells and tissue environments, which is instrumental in understanding and treating MFN2-related diseases.