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The membrane protein Dispatched (Disp), which belongs to the RND family of small molecule transporters, is essential for Hedgehog (Hh) signaling, by catalyzing the extracellular release of palmitate- and cholesterol-modified Hh ligands from producing cells. Disp function requires Furin-mediated proteolytic cleavage of its extracellular domain, but how this activates Disp remains obscure. Here, we employ cryo-electron microscopy to determine atomic structures of human Disp1 (hDisp1), before and after cleavage, and in complex with lipid-modified Sonic hedgehog (Shh) ligand. These structures, together with biochemical data, reveal that proteolytic cleavage opens the extracellular domain of hDisp1, removing steric hindrance to Shh binding. Structure-guided functional experiments demonstrate the role of hDisp1–Shh interactions in ligand release. Our results clarify the mechanisms of hDisp1 activation and Shh morphogen release, and highlight how a unique proteolytic cleavage event enabled acquisition of a protein substrate by a member of a family of small molecule transporters., Dispatched (Disp) RND transporter, activated by Furin-mediated proteolytic cleavage, mediates the release of the lipid-modified Hedgehog (Hh) ligands. Here, the authors report structures of human Disp1 (hDisp1) before and after cleavage, and in complex with lipid-modified Sonic hedgehog (Shh), with insights into the mechanisms of hDisp1 activation and function.

Plasmonic nanoantennas allow for enhancing the spontaneous emission, altering the emission polarization, and shaping the radiation pattern of quantum emitters. A critical challenge for the experimental realizations is positioning a single emitter into the hotspot of a plasmonic antenna with nanoscale accuracy. We demonstrate a dynamic light-matter interaction nanosystem enabled by the DNA origami technique. A single fluorophore molecule can autonomously and unidirectionally walk into the hotspot of a plasmonic nanoantenna along a designated origami track. Successive fluorescence intensity increase and lifetime reduction are in situ monitored using single-molecule fluorescence spectroscopy, while the fluorophore walker gradually approaches and eventually enters the plasmonic hotspot. Our scheme offers a dynamic platform, which can be used to develop functional materials, investigate intriguing light-matter interaction phenomena, and serve as prototype system for examining theoretical models.

In this paper our aim is to find the radii of starlikeness and convexity for three different kind of normalization of the $N_��(z)=az^{2}J_{��}^{\prime \prime }(z)+bzJ_{��}^{\prime}(z)+cJ_{��}(z)$ function, where $J_��(z)$ is called the Bessel function of the first kind of order $��.$ The key tools in the proof of our main results are the Mittag-Leffler expansion for $N_��(z)$ function and properties of real zeros of it. In addition, by using the Euler-Rayleigh inequalities we obtain some tight lower and upper bounds for the radii of starlikeness and convexity of order zero for the normalized $N_��(z)$ function. Finally, we evaluate certain multiple sums of the zeros for $N_��(z)$ function., 22 pages; 1 figure. arXiv admin note: text overlap with arXiv:1802.05462

The photoluminescence from aligned 7-atom wide armchair-edge graphene nanoribbons coupled to plasmonic nanoantennas was recently observed to display blinking. Photoluminescence blinking is a hallmark of emission from single quantum emitters. Here we explore the origin of the blinking. We study the influence of the local field enhancement in the vicinity of nanoantennas on the photoluminescence blinking. We observe a clear correlation between the blinking amplitudes and the plasmonic enhancement. For non-resonant metal nanostructures the blinking vanishes almost completely. Our results allow us to conclude that the blinking is an intrinsic feature of the emission from the graphene nanoribbons. This is in contrast to the case of single-molecule surface-enhanced Raman scattering, where it is known that ballistic charge transfer between plasmonic nanoparticles and the molecule under study critically contributes to the blinking.

Germin-like proteins (GLPs) are ubiquitous plant glycoproteins (belonging to the cupin super family) that play diverse roles, including abiotic stress resistance in many plant species. To identify the molecular functions underlying abiotic stress responses, the expression of germin-like protein encoding genes of soybean GmGLPs was analyzed. qRT-PCR analyses of 21 GmGLPs transcripts abundances were conducted in soybean leave tissues. The results showed that GmGLPs transcripts were highly abundant upon treatments with high salinity, PEG6000, abscisic acid (ABA) and methyl viologen (MV). The peaks of transcript copiousness induced by PEG6000 and NaCl were mostly observed after 18 h, while some genes expressed earlier than 4 h after abiotic stress treatment. A specific GmGLP7 gene, that was highly abundant under salinity, drought, ABA and MV conditions, was further characterized. The ectopic overexpression of GmGLP7 (Glyma.08G226800.1) in transgenic Arabidopsis enhanced drought, salt, and oxidative tolerance and resulted in hypersensitive phenotypes toward ABA-mediated seed germination and primary root elongation, compared to the wild-type. Taken together, these results suggest that GmGLP7 positively confers abiotic tolerance in plants.

The soilborne fungus Verticillium dahliae is the major pathogen that causes the verticillium wilt disease of plants, which leads to huge economic loss worldwide. At the early stage of infection, growth of the pathogen is subject to the nutrition stress of limited nitrogen. To investigate the secreted pathogenic proteins that play indispensable roles during invasion at this stage, we compared the profiles of secreted proteins of V. dahliae under nitrogen starvation and normal conditions by using in-gel and in-solution digestion combined with liquid chromatography–nano-electrospray ionization tandem mass spectrometry (LC–nanoESI-MS). In total, we identified 212 proteins from the supernatant of liquid medium, including 109 putative secreted proteins. Comparative analysis indicated that the expression of 76 proteins was induced, whereas that of 9 proteins was suppressed under nitrogen starvation. Notably, 24 proteins are constitutively expressed. Further bioinformatic exploration enabled us to classify the stress-induced proteins into seven functional groups: cell wall degradation (10.5%), reactive oxygen species (ROS) scavenging and stress response (11.8%), lipid effectors (5.3%), protein metabolism (21.1%), carbohydrate metabolism (15.8%), electron–proton transport and energy metabolism (14.5%), and other (21.0%). In addition, most stress-suppressed proteins are involved in the cell-wall remodeling. Taken together, our analyses provide insights into the pathogenesis of V. dahliae and might give hints for the development of novel strategy against the verticillium wilt disease.

article i nfo O-acetylserine sulfhydrylase (OASS) catalyzes the final step of cysteine biosynthesis from O-acetylserine (OAS) and inorganic sulfide in plants and bacteria. Bioinformatics analyses combined with activity assays enabled us to annotate the two putative genes of Microcystis aeruginosa PCC 7806 to CysK1 and CysK2, which encode the two 75% sequence-identical OASS paralogs. Moreover, we solved the crystal structures of CysK1 at 2.30 Ǻ and cystine-complexed CysK2 at 1.91 Ǻ, revealing a quite similar overall structure that belongs to the family of fold-type II PLP-dependent enzymes. Structural comparison indicated a significant induced fi tu pon binding to the cystine, which occupies the binding site for the substrate OAS and blocks the product release tunnel. Subsequent enzymatic assays further confirmed that cystine is a competitive inhibitor of the substrate OAS. Moreover, multiple-sequence alignment revealed that the cystine-binding residues are highly conserved in all OASS proteins, suggesting that this auto-inhibition of cystine might be a universal mechanism of cysteine biosynthesis pathway.

The fumigant toxicity of five plant essential oils (Foeniculum vulgare Miller, Lavandula stoechas L., Thymbra spicata L., Teucrium polium L. and Heracleum platytaenium Boiss.) were tested on Acanthoscelides obtectus (Say) (Col.: Bruchidae) under laboratory conditions. Single dose (100 ?l/L) of plant essential oils were initially tested on adult stage of A. obtectus. The greatest fumigant toxicity against A. obtectus was seen with F. vulgare essential oil, followed by T. spicata and L. stoechas essential oils. In the dose response bioassays with F. vulgare, T. spicata and L. stoechas, the calculated LC50 values were 22,3 ?l/L, 32,4 ?l/L and 46,3 ?l/L respectively. The main components of plant essential oils of three plants showing high response were determined by GC-MS analysis. F. vulgare essential oil's main components were anisole (79%) and L-Fenchone (13%). T. spicata and L. stoechas contain L-Fenchone (55%, 57%), Camphor (24%, 24%) and Eucalyptol (13%, 13%) respectively. Main components L-Fenchone and Camphor caused about 100% mortality at 80 ?l/L dose in 48 hours. The results indicate that F. vulgare essential oil or its components may have a potential in controlling of A. obtectus. © 2015, Entomological Society of Turkey. All rights reserved.

The situation of current research on power losses allocation in bilateral electricity markets is presented. Based on cooperative game theory, a novel nucleolus theory-based method for power losses allocation under the bilateral-transactions model is put forward and compared in detail with the Shapley-value-based allocation method. The impacts of different market players on network power losses are taken into account. With the new method, network power losses can be allocated to each transaction reasonably. The allocation results would not be affected by the sequence that each transaction is formed and be active. The method answers for the open, equal, and impartial principles of electricity market and can be easily understood and accepted by market players. Numerical tests validated the equity and validity of the method.

Carnitine is an essential cofactor for the mitochondrial beta-oxidation of long-chain fatty acids. The juvenile visceral steatosis (JVS) mouse, an animal model of systemic carnitine deficiency, is inherited in an autosomal recessive manner. Recently, a human OCTN2 gene encoding a sodium-dependent carnitine cotransporter was isolated and mapped to human chromosome 5q31. Since the mouse jvs locus was assigned to the region of chromosome 11 where it is syntenic to human chromosome 5q31, we isolated the mouse octn2 gene and screened for its mutation in the jvs mouse. DNA sequencing analysis disclosed a missense mutation from CTG (Leu) to CGG (Arg) at codon 352 located within the sixth transmembrane domain of octn2. This amino acid replacement possibly causes the conformational change of the protein that leads to dysfunction of the gene product. Hence, we conclude that octn2 is a candidate gene responsible for the JVS mouse.

The juvenile visceral steatosis (JVS) mouse exhibits hereditary systemic carnitine deficiency and develops cardiac hypertrophy. The aim of this study was to clarify the characteristics of cardiac hypertrophy in the JVS mouse. Total carnitine content in JVS mouse heart was about 10% of that of control mouse heart at 4 and 8 weeks of age. The heart weight/body weight ratio was bigger in JVS mice than that in control mice at 2 weeks of age, and this difference in ratio increased with age. The wall areas of both ventricles and septum in JVS mice were larger than those of the control mice at 2 and 8 weeks. The myocyte diameter in both ventricular walls and septum in JVS mice was longer than that of the control mice. On electron microscopy, the percent of mitochondria in the myocyte was 66% in JVS mice, and 37% in control mice. The percent of lipid fraction in JVS mice was six-fold higher than that in control mice. Total content of adenine nucleotides in JVS mouse heart was about 60% of that in control mouse heart. Adenylate energy charge in JVS mouse heart was 63 and 45% of that in the control mouse heart at 4 and 8 weeks, respectively. Overall, the cardiac enlargement observed in this animal model could be accounted for by a proportional increase in the myocyte diameter in the ventricles and septum, accompanied by an increase in mitochondria. Furthermore, this cellular growth is associated with decreases in the levels of ATP and ADP, and adenylate energy charge.

In line 12 of page 1, replace "GmGER 9" with "GmGER 15".

The long-term administration of l-carnitine was very effective in preventing cardiomegaly in juvenile visceral steatosis (JVS) mice, which was confirmed by heart weight as well as the lipid contents in heart tissue. After i.p. injection of l-carnitine, the concentration of free carnitine in heart remained constant, although serum free carnitine level increased up to 80-fold. On the other hand, a significant increase in short-chain acyl-carnitine level in heart was observed. These results suggest that increased levels of short-chain acyl-carnitine, not free carnitine, might be a key compound in the protective effect of l-carnitine administration in JVS mice.

Juvenile visceral steatosis (JVS) mice are associated with systemic carnitine deficiency (Kuwajima, et al., 1991). In order to investigate the cause of this deficiency, we compared fibroblast carnitine transport activities in normal mice and JVS mice. The kinetic analysis showed that in formal fibroblasts, the Km and Vmax values for saturable uptake was 15.6 microM and 2.56 pmol/min/mg protein, respectively. In JVS fibroblasts, however, saturable uptake was not observed. There was no great difference in the linear component of uptake between normal and JVS fibroblasts. At the physiological concentration (50 microM) of carnitine, the fibroblast carnitine transport activity in JVS mice was decreased to 18% of that in normal mice. Thus there is hardly any carnitine transport activity in the fibroblasts of JVS mice, indicating that the JVS mouse can be regarded as an animal model of primary carnitine deficiency.