Jahn-Teller stabilization of a "polar" metal oxide surface: Fe3O4(001)

Using ab initio thermodynamics we compile a phase diagram for the surface of Fe3O4(001) as a function of temperature and oxygen pressures. A hitherto ignored polar termination with octahedral iron and oxygen forming a wave-like structure along the [110]-direction is identified as the lowest energy configuration over a broad range of oxygen gas-phase conditions. This novel geometry is confirmed in a x-ray diffraction analysis. The stabilization of the Fe3O4(001)-surface goes together with dramatic changes in the electronic and magnetic properties, e.g., a halfmetal-to-metal transition.Comment: 4 pages, 4 figure

Surface electronic structure of the Fe3O4(100): Evidence of a half-metal to metal transition

In situ prepared Fe3O4(100) thin films were studied by means of scanning tunneling microscopy (STM) and spin-polarized photoelectron spectroscopy (SP-PES). The atomically resolved (2×2)R45°wavelike surface atomic structure observed by STM is explained based on density functional theory (DFT) and ab initio atomistic thermodynamics calculations as a laterally distorted surface layer containing octahedral iron and oxygen, referred to as a modified B layer. The work-function value of the Fe3O4(100) surface extracted from the cutoff of the photoelectron spectra is in good agreement with that predicted from DFT. On the Fe3O4(100) surface both the SP-PES measurements and the DFT results show a strong reduction of the spin polarization at the Fermi level (EF) compared to the bulk density of states. The nature of the states in the majority band gap of the Fe3O4 surface layer is analyzed

Dominance of virus over host factors in cross-species activation of human cytomegalovirus early gene expression

Human cytomegalovirus (HCMV) exhibits a highly restricted host range. In this study, we sought to examine the relative significance of host and viral factors in activating early gene expression of the HCMV UL54 (DNA polymerase) promoter in murine cells. Appropriate activation of the UL54 promoter at early times is essential for viral DNA replication. To study how the HCMV UL54 promoter is activated in murine cells, a transgenesis system based on yeast artificial chromosomes (YACs) was established for HCMV. A 178-kb YAC, containing a subgenomic fragment of HCMV encompassing the majority of the unique long (UL) region, was constructed by homologous recombination in yeast. This HCMV YAC backbone is defective for viral growth and lacks the major immediate-early (IE) gene region, thus permitting the analysis of essential cis-acting sequences when complemented intrans. To quantitatively measure the level of gene expression, we generated HCMV YACs containing a luciferase reporter gene inserted downstream of either the UL54 promoter or, as a control for late gene expression, the UL86 promoter, which directs expression of the major capsid protein. To determine the early gene activation pathway, point mutations were introduced into the inverted repeat 1 (IR1) element of the UL54 promoter of the HCMV YAC. In the transgenesis experiments, HCMV YACs and derivatives generated in yeast were introduced into NIH 3T3 murine cells by polyethylene glycol-mediated fusion. We found that infection of YAC, but not plasmid, transgenic lines with HCMV was sufficient to fully recapitulate the UL54 expression program at early times of infection, indicating the importance of remote regulatory elements in influencing regulation of the UL54 promoter. Moreover, YACs containing a mutant IR1 in the UL54 promoter led to reduced (∼30-fold) reporter gene expression levels, indicating that HCMV major IE gene activation of the UL54 promoter is fully permissive in murine cells. In comparison with HCMV, infection of YAC transgenic NIH 3T3 lines with murine cytomegalovirus (MCMV) resulted in lower (more than one order of magnitude) efficiency in activating UL54 early gene expression. MCMV is therefore not able to fully activate HCMV early gene expression, indicating the significance of virus over host determinants in the cross-species activation of key early gene promoters. Finally, these studies show that YAC transgenesis can be a useful tool in functional analysis of viral proteins and control of gene expression for large viral genomes

Imaging crustal structure in South-Central Costa Rica with Receiver Functions

An array of broadband seismometers transecting the Talamanca Range in southern Costa Rica was operated from 2005 until 2007. In combination with data from a short‐period network near Quepos in central Costa Rica, this data is analyzed by the receiver function method to image the crustal structure in south‐central Costa Rica. Two strong positive signals are seen in the migrated images, interpreted as the Moho (at around 35 km depth) and an intra‐crustal discontinuity (15 km depth). A relatively flat crustal and Moho interface underneath the north‐east flank of the Talamanca Range can be followed for a lateral distance of about 50 km parallel to the trench, with only slight changes in the overall geometry. Closer to the coast, the topography of the discontinuities shows several features, most notably a deeper Moho underneath the Talamanca Mountain Range and volcanic arc. Under the highest part of the mountain ranges, the Moho reaches a depth of about 50 km, which indicates that the mountain ranges are approximately isostatically compensated. Local deviations from the crustal thickness expected for isostatic equilibrium occur under the active volcanic arc and in south Costa Rica. In the transition region between the active volcanic arc and the Talamanca Range, both the Moho and intracrustal discontinuity appear distorted, possibly related to the southern edge of the active volcanic zone and deformation within the southern part of the Central Costa Rica Deformed Belt. Near the volcanoes Irazu and Turrialba, a shallow converter occurs, correlating with a low‐velocity, low‐density body seen in tomography and gravimetry. Applying a grid search for the crustal interface depth and vp/vs ratio cannot constrain vp/vs values well, but points to generally low values (<1.7) in the upper crust. This is consistent with quartz‐rich rocks forming the mountain range

Interplate seismicity at the CRISP drilling site: The 2002 Mw=6.4 Osa Earthquake at the southeastern end of the Middle America Trench

We investigate potential relations between variations in seafloor relief and age of the incoming plate and interplate seismicity. Westward from Osa Peninsula in Costa Rica, a major change in the character of the incoming Cocos Plate is displayed by abrupt lateral variations in seafloor depth and thermal structure. Here a Mw 6.4 thrust earthquake was followed by three aftershock clusters in June 2002. Initial relocations indicate that the main shock occurred fairly trenchward of most large earthquakes along the Middle America Trench off central Costa Rica. The earthquake sequence occurred while a temporary network of OBH and land stations ∼80 km to the northwest were deployed. By adding readings from permanent local stations, we obtain uncommon P wave coverage of a large subduction zone earthquake. We relocate this catalog using a nonlinear probabilistic approach within both, a 1-D and a 3-D P wave velocity models. The main shock occurred ∼25 km from the trench and probably along the plate interface at 5–10 km depth. We analyze teleseismic data to further constrain the rupture process of the main shock. The best depth estimates indicate that most of the seismic energy was radiated at shallow depth below the continental slope, supporting the nucleation of the Osa earthquake at ∼6 km depth. The location and depth coincide with the plate boundary imaged in prestack depth-migrated reflection lines shot near the nucleation area. Aftershocks propagated downdip to the area of a 1999 Mw 6.9 sequence and partially overlapped it. The results indicate that underthrusting of the young and buoyant Cocos Ridge has created conditions for interplate seismogenesis shallower and closer to the trench axis than elsewhere along the central Costa Rica margin

The steeply subducting edge of the Cocos Ridge : evidence from receiver functions beneath the northern Talamanca Range, south-central Costa Rica

The deep structure of the south-central Costa Rican subduction zone has not been studied in great detail so far because large parts of the area are virtually inaccessible. We present a receiver function study along a transect of broadband seismometers through the northern flank of the Cordillera de Talamanca (south Costa Rica). Below Moho depths, the receiver functions image a dipping positive conversion signal. This is interpreted as the subducting Cocos Plate slab, compatible with the conversions in the individual receiver functions. In finite difference modeling, a dipping signal such as the one imaged can only be reproduced by a steeply (80°) dipping structure present at least until a depth of about 70–100 km; below this depth, the length of the slab cannot be determined because of possible scattering effects. The proposed position of the slab agrees with previous results from local seismicity, local earthquake tomography, and active seismic studies, while extending the slab location to greater depths and steeper dip angle. Along the trench, no marked change is observed in the receiver functions, suggesting that the steeply dipping slab continues until the northern flank of the Cordillera de Talamanca, in the transition region between the incoming seamount segment and Cocos Ridge. Considering the time predicted for the establishment of shallow angle underthrusting after the onset of ridge collision, the southern Costa Rican subduction zone may at present be undergoing a reconfiguration of subduction style, where the transition to shallow underthrusting may be underway but still incomplete

Geodetic and seismic constraints on some seismogenic zone processes in Costa Rica

New seismic and geodetic data from Costa Rica provide insight into seismogenic zone processes in Central America, where the Cocos and Caribbean plates converge. Seismic data are from combined land and ocean bottom deployments in the Nicoya peninsula in northern Costa Rica and near the Osa peninsula in southern Costa Rica. In Nicoya, inversion of GPS data suggests two locked patches centered at 14 ± 2 and 39 ± 6 km depth. Interplate microseismicity is concentrated in the more freely slipping intermediate zone, suggesting that small interseismic earthquakes may not accurately outline the updip limit of the seismogenic zone, the rupture zone for future large earthquakes, at least over the short (∼1 year) observation period. We also estimate northwest motion of a coastal “sliver block” at 8 ± 3 mm/yr, probably related to oblique convergence. In the Osa region to the south, convergence is orthogonal to the trench. Cocos-Caribbean relative motion is partitioned here, with ∼8 cm/yr on the Cocos-Panama block boundary (including a component of permanent shortening across the Fila Costeña fold and thrust belt) and ∼1 cm/yr on the Panama block–Caribbean boundary. The GPS data suggest that the Cocos plate–Panama block boundary is completely locked from ∼10–50 km depth. This large locked zone, as well as associated forearc and back-arc deformation, may be related to subduction of the shallow Cocos Ridge and/or younger lithosphere compared to Nicoya, with consequent higher coupling and compressive stress in the direction of plate convergence

Cyclin-Dependent Kinase Activity Controls the Onset of the HCMV Lytic Cycle

The onset of human cytomegalovirus (HCMV) lytic infection is strictly synchronized with the host cell cycle. Infected G0/G1 cells support viral immediate early (IE) gene expression and proceed to the G1/S boundary where they finally arrest. In contrast, S/G2 cells can be infected but effectively block IE gene expression and this inhibition is not relieved until host cells have divided and reentered G1. During latent infection IE gene expression is also inhibited, and for reactivation to occur this block to IE gene expression must be overcome. It is only poorly understood which viral and/or cellular activities maintain the block to cell cycle or latency-associated viral IE gene repression and whether the two mechanisms may be linked. Here, we show that the block to IE gene expression during S and G2 phase can be overcome by both genotoxic stress and chemical inhibitors of cellular DNA replication, pointing to the involvement of checkpoint-dependent signaling pathways in controlling IE gene repression. Checkpoint-dependent rescue of IE expression strictly requires p53 and in the absence of checkpoint activation is mimicked by proteasomal inhibition in a p53 dependent manner. Requirement for the cyclin dependent kinase (CDK) inhibitor p21 downstream of p53 suggests a pivotal role for CDKs in controlling IE gene repression in S/G2 and treatment of S/G2 cells with the CDK inhibitor roscovitine alleviates IE repression independently of p53. Importantly, CDK inhibiton also overcomes the block to IE expression during quiescent infection of NTera2 (NT2) cells. Thus, a timely block to CDK activity not only secures phase specificity of the cell cycle dependent HCMV IE gene expression program, but in addition plays a hitherto unrecognized role in preventing the establishment of a latent-like state

Human Cytomegalovirus IE1 Protein Elicits a Type II Interferon-Like Host Cell Response That Depends on Activated STAT1 but Not Interferon-γ

Human cytomegalovirus (hCMV) is a highly prevalent pathogen that, upon primary infection, establishes life-long persistence in all infected individuals. Acute hCMV infections cause a variety of diseases in humans with developmental or acquired immune deficits. In addition, persistent hCMV infection may contribute to various chronic disease conditions even in immunologically normal people. The pathogenesis of hCMV disease has been frequently linked to inflammatory host immune responses triggered by virus-infected cells. Moreover, hCMV infection activates numerous host genes many of which encode pro-inflammatory proteins. However, little is known about the relative contributions of individual viral gene products to these changes in cellular transcription. We systematically analyzed the effects of the hCMV 72-kDa immediate-early 1 (IE1) protein, a major transcriptional activator and antagonist of type I interferon (IFN) signaling, on the human transcriptome. Following expression under conditions closely mimicking the situation during productive infection, IE1 elicits a global type II IFN-like host cell response. This response is dominated by the selective up-regulation of immune stimulatory genes normally controlled by IFN-γ and includes the synthesis and secretion of pro-inflammatory chemokines. IE1-mediated induction of IFN-stimulated genes strictly depends on tyrosine-phosphorylated signal transducer and activator of transcription 1 (STAT1) and correlates with the nuclear accumulation and sequence-specific binding of STAT1 to IFN-γ-responsive promoters. However, neither synthesis nor secretion of IFN-γ or other IFNs seems to be required for the IE1-dependent effects on cellular gene expression. Our results demonstrate that a single hCMV protein can trigger a pro-inflammatory host transcriptional response via an unexpected STAT1-dependent but IFN-independent mechanism and identify IE1 as a candidate determinant of hCMV pathogenicity

Human cytomegalovirus immediate-early 1 protein rewires upstream STAT3 to downstream STAT1 signaling switching an IL6-type to an IFNγ-like response

MN and CP were supported by the Wellcome Trust (www.wellcome.ac.uk) Institutional Strategic Support Fund and CP was supported by the Deutsche Forschungsgemeinschaft (PA 815/2-1; www.dfg.de).The human cytomegalovirus (hCMV) major immediate-early 1 protein (IE1) is best known for activating transcription to facilitate viral replication. Here we present transcriptome data indicating that IE1 is as significant a repressor as it is an activator of host gene expression. Human cells induced to express IE1 exhibit global repression of IL6- and oncostatin M-responsive STAT3 target genes. This repression is followed by STAT1 phosphorylation and activation of STAT1 target genes normally induced by IFNγ. The observed repression and subsequent activation are both mediated through the same region (amino acids 410 to 445) in the C-terminal domain of IE1, and this region serves as a binding site for STAT3. Depletion of STAT3 phenocopies the STAT1-dependent IFNγ-like response to IE1. In contrast, depletion of the IL6 receptor (IL6ST) or the STAT kinase JAK1 prevents this response. Accordingly, treatment with IL6 leads to prolonged STAT1 instead of STAT3 activation in wild-type IE1 expressing cells, but not in cells expressing a mutant protein (IE1dl410-420) deficient for STAT3 binding. A very similar STAT1-directed response to IL6 is also present in cells infected with a wild-type or revertant hCMV, but not an IE1dl410-420 mutant virus, and this response results in restricted viral replication. We conclude that IE1 is sufficient and necessary to rewire upstream IL6-type to downstream IFNγ-like signaling, two pathways linked to opposing actions, resulting in repressed STAT3- and activated STAT1-responsive genes. These findings relate transcriptional repressor and activator functions of IE1 and suggest unexpected outcomes relevant to viral pathogenesis in response to cytokines or growth factors that signal through the IL6ST-JAK1-STAT3 axis in hCMV-infected cells. Our results also reveal that IE1, a protein considered to be a key activator of the hCMV productive cycle, has an unanticipated role in tempering viral replication.Publisher PDFPeer reviewe