Spectral Modeling of SNe Ia Near Maximum Light: Probing the Characteristics of Hydro Models

We have performed detailed NLTE spectral synthesis modeling of 2 types of 1-D hydro models: the very highly parameterized deflagration model W7, and two delayed detonation models. We find that overall both models do about equally well at fitting well observed SNe Ia near to maximum light. However, the Si II 6150 feature of W7 is systematically too fast, whereas for the delayed detonation models it is also somewhat too fast, but significantly better than that of W7. We find that a parameterized mixed model does the best job of reproducing the Si II 6150 line near maximum light and we study the differences in the models that lead to better fits to normal SNe Ia. We discuss what is required of a hydro model to fit the spectra of observed SNe Ia near maximum light.Comment: 29 pages, 14 figures, ApJ, in pres

NQO1 Binds and Supports SIRT1 Function

Silent information regulator 2-related enzyme 1 (SIRT1) is an NAD+-dependent class III deacetylase and a key component of the cellular metabolic sensing pathway. The requirement of NAD+ for SIRT1 activity led us to assume that NQO1, an NADH oxidoreductase producing NAD+, regulates SIRT1 activity. We show here that SIRT1 is capable of increasing NQO1 (NAD(P)H Dehydrogenase Quinone 1) transcription and protein levels. NQO1 physically interacts with SIRT1 but not with an enzymatically dead SIRT1 H363Y mutant. The interaction of NQO1 with SIRT1 is markedly increased under mitochondrial inhibition. Interestingly, under this condition the nuclear pool of NQO1 is elevated. Depletion of NQO1 compromises the role of SIRT1 in inducing transcription of several target genes and eliminates the protective role of SIRT1 following mitochondrial inhibition. Our results suggest that SIRT1 and NQO1 form a regulatory loop where SIRT1 regulates NQO1 expression and NQO1 binds and mediates the protective role of SIRT1 during mitochondrial stress. The interplay between an NADH oxidoreductase enzyme and an NAD+ dependent deacetylase may act as a rheostat in sensing mitochondrial stress

A very low mass of Ni-56 in the ejecta of SN 1994W

We present spectroscopic and photometric observations of the luminous narrow- line Type IIP (plateau) supernova 1994W. After the plateau phase (t >120 days), the light curve dropped by 3.5 mag in V in only 12 days. Between 125 and 197 days after explosion the supernova faded substantially faster than the decay rate of Co-56, and by day 197 it was 3.6 magnitudes less luminous in R compared to SN 1987A. The low R-luminosity could indicate less than 0.0026 {+0.0017}/ {-0.0011} Msun of Ni-56 ejected at the explosion, but the emission between 125 and 197 days must then have been dominated by an additional power source, pre- sumably circumstellar interaction. Alternatively, the late light curve was dominated by Co-56 decay. In this case, the mass of the ejected Ni-56 was 0.015 {+0.012}/{-0.008} Msun, and the rapid fading between 125 and 197 days was most likely due to dust formation. Though this value of the mass is higher than in the case with the additional power source, it is still lower than estimated for any previous Type II supernova. Only progenitors with M(ZAMS) = 8-10 Msun and M(ZAMS) > 25 Msun are expected to eject such low masses of Ni-56. If M(ZAMS) = 8-10 Msun, the plateau phase indicates a low explosion energy, while for a progenitor with M(ZAMS) > 25 Msun the energy can be the canonical 1.0E{51} ergs. As SN 1994W was unusually luminous, the low-mass explosion may require an uncomfortably high efficiency in converting explosion energy into radiation. This favors a M(ZAMS) > 25 Msun progenitor. The supernova's narrow (roughly 1000 km s^{-1}) emission lines were excited by the hot supernova spectrum, rather than a circumstellar shock. The thin shell from which the lines origi- nated was most likely accelerated by the radiation from the supernova.Comment: 19 pages AASTeX v.4.0, including 5 Postscript figures; ApJ, in pres

Compromising the 19S proteasome complex protects cells from reduced flux through the proteasome

Proteasomes are central regulators of protein homeostasis in eukaryotes. Proteasome function is vulnerable to environmental insults, cellular protein imbalance and targeted pharmaceuticals. Yet, mechanisms that cells deploy to counteract inhibition of this central regulator are little understood. To find such mechanisms, we reduced flux through the proteasome to the point of toxicity with specific inhibitors and performed genome-wide screens for mutations that allowed cells to survive. Counter to expectation, reducing expression of individual subunits of the proteasome's 19S regulatory complex increased survival. Strong 19S reduction was cytotoxic but modest reduction protected cells from inhibitors. Protection was accompanied by an increased ratio of 20S to 26S proteasomes, preservation of protein degradation capacity and reduced proteotoxic stress. While compromise of 19S function can have a fitness cost under basal conditions, it provided a powerful survival advantage when proteasome function was impaired. This means of rebalancing proteostasis is conserved from yeast to humans

Non-Native Forest Tree Species in Europe: The Question of Seed Origin in Afforestation

Non-native forest tree species have been introduced in Europe since the 16th century, but only in the second half of the 20th century the significance of the seed source origin for their economic use was recognized, resulting in the establishment of numerous provenance trials at a national, regional, European and International level, as those led by IUFRO. Breeding programs have also been launched in the continent for the most economically important species. Aim of this work is the formulation of provenance recommendations for planting of five non-native tree species in Europe (Douglas fir, grand fir, Sitka spruce, lodgepole pine and black locust), based on the information obtained from twenty countries, in the frame of the EU FP-1403 NNEXT Cost Action. The survey revealed that official and non-official national recommendations, based on provenance research results, have been elaborated and followed at a different level and extend for the above five species, but only for Douglas fir recommendations exist in almost all the participating to the survey countries. The compilation of provenance recommendations across Europe for each species is presented in the current work. Besides the recommended introduced seed sources, European seed sources are also preferred for planting, due to ease of access and high availability of forest reproductive material. European breeding programs yielding genetic material of high productivity and quality constitute currently the seed source of choice for several species and countries. Consolidation of trial data obtained across countries will allow the joint analysis that is urgently needed to draw solid conclusions, and will facilitate the development of ‘Universal-Response-Functions’ for the species of interest, rendering possible the identification of the genetic material suitable for global change. New provenance trial series that will test seed sources from the entire climatic range of the species, established in sites falling within and outside the environmental envelopes of their natural ranges, are urgently needed to pinpoint and understand the species-specific climate constraints, as well as to correlate functional traits to the seed origin and the environmental conditions of the test sites, so that the selection of suitable forest reproductive material of non-native tree species in the face of climate change can be feasible.publishedVersio

Monitoring of species’ genetic diversity in Europe varies greatly and overlooks potential climate change impacts

Genetic monitoring of populations currently attracts interest in the context of the Convention on Biological Diversity but needs long-term planning and investments. However, genetic diversity has been largely neglected in biodiversity monitoring, and when addressed, it is treated separately, detached from other conservation issues, such as habitat alteration due to climate change. We report an accounting of efforts to monitor population genetic diversity in Europe (genetic monitoring effort, GME), the evaluation of which can help guide future capacity building and collaboration towards areas most in need of expanded monitoring. Overlaying GME with areas where the ranges of selected species of conservation interest approach current and future climate niche limits helps identify whether GME coincides with anticipated climate change effects on biodiversity. Our analysis suggests that country area, financial resources and conservation policy influence GME, high values of which only partially match species’ joint patterns of limits to suitable climatic conditions. Populations at trailing climatic niche margins probably hold genetic diversity that is important for adaptation to changing climate. Our results illuminate the need in Europe for expanded investment in genetic monitoring across climate gradients occupied by focal species, a need arguably greatest in southeastern European countries. This need could be met in part by expanding the European Union’s Birds and Habitats Directives to fully address the conservation and monitoring of genetic diversity

The ALICE experiment at the CERN LHC

ALICE (A Large Ion Collider Experiment) is a general-purpose, heavy-ion detector at the CERN LHC which focuses on QCD, the strong-interaction sector of the Standard Model. It is designed to address the physics of strongly interacting matter and the quark-gluon plasma at extreme values of energy density and temperature in nucleus-nucleus collisions. Besides running with Pb ions, the physics programme includes collisions with lighter ions, lower energy running and dedicated proton-nucleus runs. ALICE will also take data with proton beams at the top LHC energy to collect reference data for the heavy-ion programme and to address several QCD topics for which ALICE is complementary to the other LHC detectors. The ALICE detector has been built by a collaboration including currently over 1000 physicists and engineers from 105 Institutes in 30 countries. Its overall dimensions are 161626 m3 with a total weight of approximately 10 000 t. The experiment consists of 18 different detector systems each with its own specific technology choice and design constraints, driven both by the physics requirements and the experimental conditions expected at LHC. The most stringent design constraint is to cope with the extreme particle multiplicity anticipated in central Pb-Pb collisions. The different subsystems were optimized to provide high-momentum resolution as well as excellent Particle Identification (PID) over a broad range in momentum, up to the highest multiplicities predicted for LHC. This will allow for comprehensive studies of hadrons, electrons, muons, and photons produced in the collision of heavy nuclei. Most detector systems are scheduled to be installed and ready for data taking by mid-2008 when the LHC is scheduled to start operation, with the exception of parts of the Photon Spectrometer (PHOS), Transition Radiation Detector (TRD) and Electro Magnetic Calorimeter (EMCal). These detectors will be completed for the high-luminosity ion run expected in 2010. This paper describes in detail the detector components as installed for the first data taking in the summer of 2008

Degradation of Intrinsically Disordered Proteins by the NADH 26S Proteasome

The 26S proteasome is the endpoint of the ubiquitin- and ATP-dependent degradation pathway. Over the years, ATP was regarded as completely essential for 26S proteasome function due to its role in ubiquitin-signaling, substrate unfolding and ensuring its structural integrity. We have previously reported that physiological concentrations of NADH are efficient in replacing ATP to maintain the integrity of an enzymatically functional 26S PC. However, the substrate specificity of the NADH-stabilized 26S proteasome complex (26S PC) was never assessed. Here, we show that the binding of NADH to the 26S PC inhibits the ATP-dependent and ubiquitin-independent degradation of the structured ODC enzyme. Moreover, the NADH-stabilized 26S PC is efficient in degrading intrinsically disordered protein (IDP) substrates that might not require ATP-dependent unfolding, such as p27, Tau, c-Fos and more. In some cases, NADH-26S proteasomes were more efficient in processing IDPs than the ATP-26S PC. These results indicate that in vitro, physiological concentrations of NADH can alter the processivity of ATP-dependent 26S PC substrates such as ODC and, more importantly, the NADH-stabilized 26S PCs promote the efficient degradation of many IDPs. Thus, ATP-independent, NADH-dependent 26S proteasome activity exemplifies a new principle of how mitochondria might directly regulate 26S proteasome substrate specificity