A novel function for the Caenorhabditis elegans torsin OOC-5 in nucleoporin localization and nuclear import.

Torsin proteins are AAA+ ATPases that localize to the endoplasmic reticular/nuclear envelope (ER/NE) lumen. A mutation that markedly impairs torsinA function causes the CNS disorder DYT1 dystonia. Abnormalities of NE membranes have been linked to torsinA loss of function and the pathogenesis of DYT1 dystonia, leading us to investigate the role of the Caenorhabditis elegans torsinA homologue OOC-5 at the NE. We report a novel role for torsin in nuclear pore biology. In ooc-5-mutant germ cell nuclei, nucleoporins (Nups) were mislocalized in large plaques beginning at meiotic entry and persisted throughout meiosis. Moreover, the KASH protein ZYG-12 was mislocalized in ooc-5 gonads. Nups were mislocalized in adult intestinal nuclei and in embryos from mutant mothers. EM analysis revealed vesicle-like structures in the perinuclear space of intestinal and germ cell nuclei, similar to defects reported in torsin-mutant flies and mice. Consistent with a functional disruption of Nups, ooc-5-mutant embryos displayed impaired nuclear import kinetics, although the nuclear pore-size exclusion barrier was maintained. Our data are the first to demonstrate a requirement for a torsin for normal Nup localization and function and suggest that these functions are likely conserved

The Frustration with Utilization: Why Have Improvements in Internal Phosphorus Utilization Efficiency in Crops Remained so Elusive?

Despite the attention internal phosphorus utilization efficiency (PUE) of crops has received in the literature, little progress in breeding crop cultivars with high PUE has been made. Surprisingly few studies have specifically investigated PUE; instead, genotypic variation for PUE has been investigated in studies that concurrently assess phosphorus acquisition efficiency (PAE). We hypothesized that genotypic differences in PAE confound PUE rankings because genotypes with higher PAE suffer a lower degree of P stress, resulting in lower PUE. The hypothesis was tested by comparing soil-based screening to a modified technique whereby rice genotypes were grown in individual containers with a single dose of solution P, to eliminate differences in P uptake among genotypes. Genotypic differences in PUE were apparent in root and shoot tissue using the modified nutrient solution technique, but PUE rankings showed no correlation with those from traditional soil-based screening. We conclude that PUE in soil-based screening systems is unavoidably linked with genotypic PAE, resulting in PUE rankings confounded by differences in P uptake. Only screening techniques assuring equal P uptake are suitable for the exploitation of genotypic variation for PUE

The nuclear envelope localization of DYT1 dystonia torsinA-ΔE requires the SUN1 LINC complex component

<p>Abstract</p> <p>Background</p> <p>DYT1 dystonia is an autosomal dominant neurological condition caused by a mutation that removes a single glutamic acid residue (ΔE) from the torsinA (torA) AAA+ protein. TorA appears to possess a nuclear envelope (NE) localized activity that requires Lamina-Associated-Polypeptide 1 (LAP1), which is an inner nuclear membrane localized torA-binding partner. Although hypoactive, the DYT1 dystonia torA-ΔE isoform often concentrates in the NE, suggesting that torA-ΔE also interacts with an NE-localized binding partner.</p> <p>Results</p> <p>We confirm that NE-localized torA-ΔE does not co-immunoprecipitate with LAP1, and find that torA-ΔE continues to concentrate in the NE of cells that lack LAP1. Instead, we find that variability in torA-ΔE localization correlates with the presence of the SUN-domain and Nesprin proteins that assemble into the LINC complex. We also find that siRNA depletion of SUN1, but not other LINC complex components, removes torA-ΔE from the NE. In contrast, the LAP1-dependent NE-accumulation of an ATP-locked torA mutant is unaffected by loss of LINC complex proteins. This SUN1 dependent torA-ΔE localization requires the torA membrane association domain, as well as a putative substrate-interaction residue, Y147, neither of which are required for torA interaction with LAP1. We also find that mutation of these motifs, or depletion of SUN1, decreases the amount of torA-WT that colocalizes with NE markers, indicating that each also underlies a normal NE-localized torA binding interaction.</p> <p>Conclusions</p> <p>These data suggest that the disease causing ΔE mutation promotes an association between torA and SUN1 that is distinct to the interaction between LAP1 and ATP-bound torA. This evidence for two NE-localized binding partners suggests that torA may act on multiple substrates and/or possesses regulatory co-factor partners. In addition, finding that the DYT1 mutation causes abnormal association with SUN1 implicates LINC complex dysfunction in DYT1 dystonia pathogenesis, and suggests a gain-of-function activity contributes to this dominantly inherited disease.</p

MODELING JET INTERACTIONS WITH THE AMBIENT MEDIUM

Recent high-resolution (see, e.g., [13]) observations of astrophysical jets reveal complex structures apparently caused by ejecta from the central engine as the ejecta interact with the surrounding interstellar material. These observations include time-lapsed “movies” of both AGN and microquasars jets which also show that the jet phenomena are highly time-dependent. Such observations can be used to inform models of the jet–ambient-medium interactions. Based on an analysis of these data, we posit that a significant part of the observed phenomena come from the interaction of the ejecta with prior ejecta as well as interstellar material. In this view, astrophysical jets interact with the ambient medium through which they propagate, entraining and accelerating it. We show some elements of the modeling of these jets in this paper, including energy loss and heating via plasma processes, and large scale hydrodynamic and relativistic hydrodynamic simulations

Multiscale Modeling of Astrophysical Jets

We are developing the capability for a multi-scale code to model the energy deposition rate and momentum transfer rate of an astrophysical jet which generates strong plasma turbulence in its interaction with the ambient medium through which it propagates. We start with a highly parallelized version of the VH-1 Hydrodynamics Code (Coella and Wood 1984, and Saxton et al., 2005). We are also considering the PLUTO code (Mignone et al. 2007) to model the jet in the magnetohydrodynamic (MHD) and relativistic, magnetohydrodynamic (RMHD) regimes. Particle-in-Cell approaches are also being used to benchmark a wave-population models of the two-stream instability and associated plasma processes in order to determine energy deposition and momentum transfer rates for these modes of jet-ambient medium interactions. We show some elements of the modeling of these jets in this paper, including energy loss and heating via plasma processes, and large scale hydrodynamic and relativistic hydrodynamic simulations. A preliminary simulation of a jet from the galactic center region is used to lend credence to the jet as the source of the so-called the Fermi Bubble (see, e.g., Su, M. &amp; Finkbeiner, D. P., 2012)*It is with great sorrow that we acknowledge the loss of our colleague and friend of more than thirty years, Dr. John Ural Guillory, to his battle with cancer