Retention of water in terrestrial magma oceans and carbon-rich early atmospheres

Massive steam and CO$_2$ atmospheres have been proposed for magma ocean outgassing of Earth and terrestrial planets. Yet formation of such atmospheres depends on volatile exchange with the molten interior, governed by volatile solubilities and redox reactions. We determine the evolution of magma ocean--atmosphere systems for a range of oxygen fugacities, C/H ratios and hydrogen budgets that include redox reactions for hydrogen (H$_2$--H$_2$O), carbon (CO--CO$_2$), methane (CH$_4$), and solubility laws for H$_2$O and CO$_2$. We find that small initial budgets of hydrogen, high C/H ratios, and oxidizing conditions, suppress outgassing of hydrogen until the late stage of magma ocean crystallization. Hence early atmospheres in equilibrium with magma oceans are dominantly carbon-rich, and specifically CO-rich except at the most oxidizing conditions. The high solubility of H$_2$O limits its outgassing to melt fractions below $\sim$30\%, the fraction at which the mantle transitions from vigorous to sluggish convection with melt percolation. Sluggish melt percolation could enable a surface lid to form, trapping water in the interior and thereby maintaining a carbon-rich atmosphere (equilibrium crystallization). Alternatively, efficient crystal settling could maintain a molten surface, promoting a transition to a water-rich atmosphere (fractional crystallization). However, additional processes, including melt trapping and H dissolution in crystallizing minerals, further conspire to limit the extent of H outgassing, even for fractional crystallization. Hence, much of the water delivered to planets during their accretion can be safely harbored in their interiors during the magma ocean stage, particularly at oxidizing conditions.Comment: 35 pages, 16 figures, accepted version in The Planetary Science Journa

Timescales of chemical equilibrium between the convecting solid mantle and over- and underlying magma oceans

After accretion and formation, terrestrial planets go through at least one magma ocean episode. As the magma ocean crystallises, it creates the first layer of solid rocky mantle. Two different scenarios of magma ocean crystallisation involve that the solid mantle either (1) first appears at the core–mantle boundary and grows upwards or (2) appears at mid-mantle depth and grows in both directions. Regardless of the magma ocean freezing scenario, the composition of the solid mantle and liquid reservoirs continuously change due to fractional crystallisation. This chemical fractionation has important implications for the long-term thermo-chemical evolution of the mantle as well as its present-day dynamics and composition. In this work, we use numerical models to study convection in a solid mantle bounded at one or both boundaries by magma ocean(s) and, in particular, the related consequences for large-scale chemical fractionation. We use a parameterisation of fractional crystallisation of the magma ocean(s) and (re)melting of solid material at the interface between these reservoirs. When these crystallisation and remelting processes are taken into account, convection in the solid mantle occurs readily and is dominated by large wavelengths. Related material transfer across the mantle–magma ocean boundaries promotes chemical equilibrium and prevents extreme enrichment of the last-stage magma ocean (as would otherwise occur due to pure fractional crystallisation). The timescale of equilibration depends on the convective vigour of mantle convection and on the efficiency of material transfer between the solid mantle and magma ocean(s). For Earth, this timescale is comparable to that of magma ocean crystallisation suggested in previous studies (Lebrun et al., 2013), which may explain why the Earth's mantle is rather homogeneous in composition, as supported by geophysical constraints

Posttranscriptional regulation of PARG mRNA by HuR facilitates DNA repair and resistance to PARP inhibitors

The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9–mediated silencing of the HuR locus increases the relative sensitivity of PDAC cells to PARP inhibitors (PARPi). PDAC cells treated with PARPi stimulated translocation of HuR from the nucleus to the cytoplasm, specifically promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (PARG) mRNA, by binding a unique sequence embedded in its 30 untranslated region. HuR-dependent upregulation of PARG expression facilitated DNA repair via hydrolysis of polyADP-ribose on related repair proteins. Accordingly, strategies to inhibit HuR directly promoted DNA damage accumulation, inefficient PAR removal, and persistent PARP-1 residency on chromatin (PARP-1 trapping). Immunoprecipitation assays demonstrated that the PARP-1 protein binds and posttranslationally modifies HuR in PARPi-treated PDAC cells. In a mouse xenograft model of human PDAC, PARPi monotherapy combined with targeted silencing of HuR significantly reduced tumor growth compared with PARPi therapy alone. Our results highlight the HuR–PARG axis as an opportunity to enhance PARPi-based therapies. ©2017 AACR

Sanitation and Health

As one article in a four-part PLoS Medicine series on water and sanitation, David Trouba and colleagues discuss the importance of improved sanitation to health and the role that the health sector can play in its advocacy

Nef-mediated Clathrin-coated Pit Formation

The sequence of events leading to clathrin-coated pit (CCP) nucleation on the cell surface and to the incorporation of receptors into these endocytic structures is still imperfectly understood. In particular, the question remains as to whether receptor tails initiate the assembly of the coat proteins or whether receptors migrate into preformed CCP. This question was approached through a dissection of the mechanisms implemented by Nef, an early protein of human and simian immunodeficiency virus (HIV and SIV, respectively), to accelerate the endocytosis of cluster of differentiation antigen type 4 (CD4), the major receptor for these viruses. Results collected showed that: (a) Nef promotes CD4 internalization via an increased association of CD4 with CCP; (b) the Nef-mediated increase of CD4 association with CCP is related to a doubling of the plasma membrane area occupied by clathrin-coated structures; (c) this increased CCP number at the plasma membrane has functional consequences preferentially on CD4 uptake and does not significantly affect transferrin receptor internalization or fluid-phase endocytosis; (d) the presence of a CD4 cytoplasmic tail including a critical dileucine motif is required to induce CCP formation via Nef; and (e) when directly anchored to the cytoplasmic side of the plasma membrane, Nef itself can promote CCP formation. Taken together, these observations lead us to propose that CD4 can promote CCP generation via the connector molecule Nef. In this model, Nef interacts on one side with CD4 through a dileucine-based motif present on CD4 cytoplasmic tail and on the other side with components of clathrin-coated surface domain (i.e., adaptins). These Nef-generated complexes would then initiate the nucleation of CCP