180 research outputs found

    The seed testing station's role in the testing of fungicides

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    Who is adjusting to whom?: Differences in elephant diel activity in wildlife corridors across different human-modified landscapes

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    The global impact of increased human activities has consequences on the conservation of wildlife. Understanding how wildlife adapts to increased human pressures with urban expansion and agricultural areas is fundamental to future conservation plans of any species. However, there is a belief that large wild free-ranging carnivores and ungulates, cannot coexist with people, limited studies have looked at wildlife movements through differing human-dominated landscapes at finer spatial scales, in Africa. This information is vital as the human population is only going to increase and the wildlife protected areas decrease. We used remote-sensor camera traps to identify the movement patterns of African elephant (Loxodonta africana) through six wildlife corridors in Botswana. The wildlife corridors were located in two different human-dominated landscapes (agricultural/urban), with varying degrees of human impact. While we found that elephants use corridors in both landscapes, they use the urban corridors both diurnally and nocturnally in contrast to agricultural corridors which were only nocturnal. Our results provide evidence for temporal partitioning of corridor use by elephants. We identified that seasonality and landscape were important factors in determining the presence of elephants in the corridors. Our findings demonstrate that elephant diel patterns of use of the wildlife corridor differs based on the surrounding human land-uses on an hourly basis and daily basis, revealing potential adaptation and risk avoidance behaviour

    SUMOylation by Pias1 Regulates the Activity of the Hedgehog Dependent Gli Transcription Factors

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    Hedgehog (Hh) signaling, a vital signaling pathway for the development and homeostasis of vertebrate tissues, is mediated by members of the Gli family of zinc finger transcription factors. Hh signaling increases the transcriptional activity of Gli proteins, at least in part, by inhibiting their proteolytic processing. Conversely, phosphorylation by cAMP-dependent protein kinase (PKA) inhibits Gli transcriptional activity by promoting their ubiquitination and proteolysis. Whether other post-translational modifications contribute to the regulation of Gli protein activity has been unclear.Here we provide evidence that all three Gli proteins are targets of small ubiquitin-related modifier (SUMO)-1 conjugation. Expression of SUMO-1 or the SUMO E3 ligase, Pias1, increased Gli transcriptional activity in cultured cells. Moreover, PKA activity reduced Gli protein SUMOylation. Strikingly, in the embryonic neural tube, the forced expression of Pias1 increased Gli activity and induced the ectopic expression of the Gli dependent gene Nkx2.2. Conversely, a point mutant of Pias1, that lacks ligase activity, blocked the endogenous expression of Nkx2.2.Together, these findings provide evidence that Pias1-dependent SUMOylation influences Gli protein activity and thereby identifies SUMOylation as a post-translational mechanism that regulates the hedgehog signaling pathway

    Intermittency of near-bottom turbulence in tidal flow on a shallow shelf

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    The higher-order structure functions of vertical velocity fluctuations (transverse structure functions (TSF)) were employed to study the characteristics of turbulence intermittency in a reversing tidal flow on a 19 m deep shallow shelf of the East China Sea. Measurements from a downward-looking, bottom-mounted Acoustic Doppler Velocimeter, positioned 0.45 m above the seafloor, which spanned two semidiurnal tidal cycles, were analyzed. A classical lognormal single-parameter (mu) model for intermittency and the universal multifractal approach (specifically, the two-parameter (C-1 and alpha) log-Levy model) were employed to analyze the TSF exponent xi(q) in tidally driven turbulent boundary layer and to estimate mu, C-1, and alpha. During the energetic flooding tidal phases, the parameters of intermittency models approached the mean values of (mu) over tilde approximate to 0.24, (C) over tilde (1) approximate to 0.15, and (alpha) over tilde approximate to 1.5, which are accepted as the universal values for fully developed turbulence at high Reynolds numbers. With the decrease of advection velocity, mu and C-1 increased up to mu approximate to 0.5-0.6 and C-1 approximate to 0.25-0.35, but a decreased to about 1.4. The results explain the reported disparities between the smaller "universal" values of intermittency parameters mu and C-1 (mostly measured in laboratory and atmospheric high Reynolds number flows) and those (mu = 0.4-0.5) reported for oceanic stratified turbulence in the pycnocline, which is associated with relatively low local Reynolds numbers R-lambda w. The scaling exponents xi(2) of the second-order TSF, relative to the third-order structure function, was also found to be a decreasing function of R-lambda w, approaching the classical value of 2/3 only at very high R-lambda w. A larger departure from the universal turbulent regime at lower Reynolds numbers could be attributed to the higher anisotropy and associated intermittency of underdeveloped turbulence.U.S. Office of Naval Research [N00014-05-1-0245]; Spanish Ministry of Education and Science [FIS2008-03608]; Major State Program of China for Basic Research [2006CB400602]; Catalan Institute for Water Research (ICRA

    Point Mutations in GLI3 Lead to Misregulation of its Subcellular Localization

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    Background Mutations in the transcription factor GLI3, a downstream target of Sonic Hedgehog (SHH) signaling, are responsible for the development of malformation syndromes such as Greig-cephalopolysyndactyly-syndrome (GCPS), or Pallister-Hall-syndrome (PHS). Mutations that lead to loss of function of the protein and to haploinsufficiency cause GCPS, while truncating mutations that result in constitutive repressor function of GLI3 lead to PHS. As an exception, some point mutations in the C-terminal part of GLI3 observed in GCPS patients have so far not been linked to loss of function. We have shown recently that protein phosphatase 2A (PP2A) regulates the nuclear localization and transcriptional activity a of GLI3 function. Principal Findings We have shown recently that protein phosphatase 2A (PP2A) and the ubiquitin ligase MID1 regulate the nuclear localization and transcriptional activity of GLI3. Here we show mapping of the functional interaction between the MID1-α4-PP2A complex and GLI3 to a region between amino acid 568-1100 of GLI3. Furthermore we demonstrate that GCPS-associated point mutations, that are located in that region, lead to misregulation of the nuclear GLI3-localization and transcriptional activity. GLI3 phosphorylation itself however appears independent of its localization and remains untouched by either of the point mutations and by PP2A-activity, which suggests involvement of an as yet unknown GLI3 interaction partner, the phosphorylation status of which is regulated by PP2A activity, in the control of GLI3 subcellular localization and activity. Conclusions The present findings provide an explanation for the pathogenesis of GCPS in patients carrying C-terminal point mutations, and close the gap in our understanding of how GLI3-genotypes give rise to particular phenotypes. Furthermore, they provide a molecular explanation for the phenotypic overlap between Opitz syndrome patients with dysregulated PP2A-activity and syndromes caused by GLI3-mutations
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