Effects of salinity on establishment of Populus fremontii (cottonwood) and Tamarix ramosissima (saltcedar) in southwestern United States

The exotic shrub Tamarix ramosissima (saltcedar) has replaced the native Populus fremontii (cottonwood) along many streams in southwestern United States. We used a controlled outdoor experiment to examine the influence of river salinity on germination and first year survival of P. fremontii var. wislizenii (Rio Grande cottonwood) and T. ramosissima on freshly deposited alluvial bars. We grew both species from seed in planters of sand subjected to a declining water table and solutions containing 0, 1, 3, and 5 times the concentrations of major ions in the Rio Grande at San Marcia, NM (1.2, 10.0, 25.7 and 37.4 meq 1 -1 ; 0.11, 0.97, 2.37, and 3.45 dS m -1 ). Germination of P. fremontii declined by 35% with increasing salinity ( P = .008). Germination of T. ramosissima was not affected. There were no significant effects of salinity on morality or above- and belowground growth of either species. In laboratory tests the same salinities had no effect on P. fremontii germination. P. fremontii germination is more sensitive to salinity outdoors than in covered petri dishes, probably because water scarcity resulting from eavaportion intensifies the low soil water potential associated with high salinity. River salinity appears to play only a minor role in determining relative numbers of P. fremontii and T. ramosissima seedlings on freshly deposited sandbars. However, over many years salt becomes concentrated on floodplains as a result of evaporation and salt extrusion from saltcedar leaves. T. ramosissima is known to be more tolerant of the resulting extreme salinities than P. fremontii . Therefore, increases in river salinities could indirectly contribute to decline of P. fremontii forests by exacerbating salt accumulation on floodplains.     

Modelling the rheology of MgO under Earth's mantle pressure, temperature and strain rates

Plate tectonics, which shapes the surface of Earth, is the result of solid-state convection in Earth's mantle over billions of years. Simply driven by buoyancy forces, mantle convection is complicated by the nature of the convecting materials, which are not fluids but polycrystalline rocks. Crystalline materials can flow as the result of the motion of defects--point defects, dislocations, grain boundaries and so on. Reproducing in the laboratory the extreme deformation conditions of the mantle is extremely challenging. In particular, experimental strain rates are at least six orders of magnitude larger than in nature. Here we show that the rheology of MgO at the pressure, temperature and strain rates of the mantle is accessible by multiscale numerical modelling starting from first principles and with no adjustable parameters. Our results demonstrate that extremely low strain rates counteract the influence of pressure. In the mantle, MgO deforms in the athermal regime and this leads to a very weak phase. It is only in the lowermost lower mantle that the pressure effect could dominate and that, under the influence of lattice friction, a viscosity of the order of 10(21)-10(22) pascal seconds can be defined for MgO.     

Fast core rotation in red-giant stars as revealed by gravity-dominated mixed modes

When the core hydrogen is exhausted during stellar evolution, the central region of a star contracts and the outer envelope expands and cools, giving rise to a red giant. Convection takes place over much of the star's radius. Conservation of angular momentum requires that the cores of these stars rotate faster than their envelopes; indirect evidence supports this. Information about the angular-momentum distribution is inaccessible to direct observations, but it can be extracted from the effect of rotation on oscillation modes that probe the stellar interior. Here we report an increasing rotation rate from the surface of the star to the stellar core in the interiors of red giants, obtained using the rotational frequency splitting of recently detected 'mixed modes'. By comparison with theoretical stellar models, we conclude that the core must rotate at least ten times faster than the surface. This observational result confirms the theoretical prediction of a steep gradient in the rotation profile towards the deep stellar interior.     

DCC constrains tumour progression via its dependence receptor activity

The role of deleted in colorectal carcinoma (DCC) as a tumour suppressor has been a matter of debate for the past 15 years. DCC gene expression is lost or markedly reduced in the majority of advanced colorectal cancers and, by functioning as a dependence receptor, DCC has been shown to induce apoptosis unless engaged by its ligand, netrin-1 (ref. 2). However, so far no animal model has supported the view that the DCC loss-of-function is causally implicated as predisposing to aggressive cancer development. To investigate the role of DCC-induced apoptosis in the control of tumour progression, here we created a mouse model in which the pro-apoptotic activity of DCC is genetically silenced. Although the loss of DCC-induced apoptosis in this mouse model is not associated with a major disorganization of the intestines, it leads to spontaneous intestinal neoplasia at a relatively low frequency. Loss of DCC-induced apoptosis is also associated with an increase in the number and aggressiveness of intestinal tumours in a predisposing APC mutant context, resulting in the development of highly invasive adenocarcinomas. These results demonstrate that DCC functions as a tumour suppressor via its ability to trigger tumour cell apoptosis.     

XIAP deficiency in humans causes an X-linked lymphoproliferative syndrome

The homeostasis of the immune response requires tight regulation of the proliferation and apoptosis of activated lymphocytes. In humans, defects in immune homeostasis result in lymphoproliferation disorders including autoimmunity, haemophagocytic lymphohystiocytosis and lymphomas. The X-linked lymphoproliferative syndrome (XLP) is a rare, inherited immunodeficiency that is characterized by lymphohystiocytosis, hypogammaglobulinaemia and lymphomas, and that usually develops in response to infection with Epstein-Barr virus (EBV). Mutations in the signalling lymphocyte activation molecule (SLAM)-associated protein SAP, a signalling adaptor molecule, underlie 60% of cases of familial XLP. Here, we identify mutations in the gene that encodes the X-linked inhibitor-of-apoptosis XIAP (also termed BIRC4) in patients with XLP from three families without mutations in SAP. These mutations lead to defective expression of XIAP. We show that apoptosis of lymphocytes from XIAP-deficient patients is enhanced in response to various stimuli including the T-cell antigen receptor (TCR)-CD3 complex, the death receptor CD95 (also termed Fas or Apo-1) and the TNF-associated apoptosis-inducing ligand receptor (TRAIL-R). We also found that XIAP-deficient patients, like SAP-deficient patients, have low numbers of natural killer T-lymphocytes (NKT cells), indicating that XIAP is required for the survival and/or differentiation of NKT cells. The observation that XIAP-deficiency and SAP-deficiency are both associated with a defect in NKT cells strengthens the hypothesis that NKT cells have a key role in the immune response to EBV. Furthermore, by identifying an XLP immunodeficiency that is caused by mutations in XIAP, we show that XIAP is a potent regulator of lymphocyte homeostasis in vivo.     

Karyopherin-mediated import of integral inner nuclear membrane proteins

Targeting of newly synthesized integral membrane proteins to the appropriate cellular compartment is specified by discrete sequence elements, many of which have been well characterized. An understanding of the signals required to direct integral membrane proteins to the inner nuclear membrane (INM) remains a notable exception. Here we show that integral INM proteins possess basic sequence motifs that resemble 'classical' nuclear localization signals. These sequences can mediate direct binding to karyopherin-alpha and are essential for the passage of integral membrane proteins to the INM. Furthermore, karyopherin-alpha, karyopherin-beta1 and the Ran GTPase cycle are required for INM targeting, underscoring parallels between mechanisms governing the targeting of integral INM proteins and soluble nuclear transport. We also provide evidence that specific nuclear pore complex proteins contribute to this process, suggesting a role for signal-mediated alterations in the nuclear pore complex to allow for passage of INM proteins along the pore membrane.     

Enhanced bacterial clearance and sepsis resistance in caspase-12-deficient mice

Caspases function in both apoptosis and inflammatory cytokine processing and thereby have a role in resistance to sepsis. Here we describe a novel role for a caspase in dampening responses to bacterial infection. We show that in mice, gene-targeted deletion of caspase-12 renders animals resistant to peritonitis and septic shock. The resulting survival advantage was conferred by the ability of the caspase-12-deficient mice to clear bacterial infection more efficiently than wild-type littermates. Caspase-12 dampened the production of the pro-inflammatory cytokines interleukin (IL)-1beta, IL-18 (interferon (IFN)-gamma inducing factor) and IFN-gamma, but not tumour-necrosis factor-alpha and IL-6, in response to various bacterial components that stimulate Toll-like receptor and NOD pathways. The IFN-gamma pathway was crucial in mediating survival of septic caspase-12-deficient mice, because administration of neutralizing antibodies to IFN-gamma receptors ablated the survival advantage that otherwise occurred in these animals. Mechanistically, caspase-12 associated with caspase-1 and inhibited its activity. Notably, the protease function of caspase-12 was not necessary for this effect, as the catalytically inactive caspase-12 mutant Cys299Ala also inhibited caspase-1 and IL-1beta production to the same extent as wild-type caspase-12. In this regard, caspase-12 seems to be the cFLIP counterpart for regulating the inflammatory branch of the caspase cascade. In mice, caspase-12 deficiency confers resistance to sepsis and its presence exerts a dominant-negative suppressive effect on caspase-1, resulting in enhanced vulnerability to bacterial infection and septic mortality.