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The complexity of mechanisms driving protein sorting into exosomes is only beginning to emerge. In a paper recently published in Cell Research, Roucourt et al. report that trimming of heparan sulfate side chains of syndecans by cndosomal heparanase facilitates sorting into exosomes by the formation of tight syndecan clusters that are recruited by the multivalent adaptor syntenin to the ALIX-ESCRT sorting machinery at endosomes.

Subcellular trafficking is required for a multitude of functions in eukaryotic cells. It involves regulation of cargo sorting, vesicle formation, trafficking and fusion processes at multiple levels. Adaptor protein （AP） complexes are key regulators of cargo sorting into vesicles in yeast and mammals but their existence and function in plants have not been demonstrated. Here we report the identification of the protein-affected trafficking 4 （pat4） mutant defective in the putative 6 subunit of the AP-3 complex, pat4 and pat2, a mutant isolated from the same GFP imaging-based for- ward genetic screen that lacks a functional putative AP-3 β, as well as dominant negative AP-3 μ transgenic lines dis- play undistinguishable phenotypes characterized by largely normal morphology and development, but strong intra- cellular accumulation of membrane proteins in aberrant vacuolar structures. All mutants are defective in morphol- ogy and function of lytic and protein storage vacuoles （PSVs） but show normal sorting of reserve proteins to PSVs. Immunoprecipitation experiments and genetic studies revealed tight functional and physical associations of putative AP-3 β and AP-3 δ subunits. Furthermore, both proteins are closely linked with putative AP-3μvand σ subunits and several components of the clathrin and dynamin machineries. Taken together, these results demonstrate that AP complexes, similar to those in other eukaryotes, exist in plants, and that AP-3 plays a specific role in the regulation of biogenesis and function of vacuoles in plant ceils.

IRTKS encodes a member of the IRSp53/MIM homology domain family, which has been shown to play an im- portant role in the formation of plasma membrane protrusions. Although the phosphorylation of IRTKS occurs in response to insulin stimulation, the role of this protein in insulin signaling remains unknown. Here we show that IRTKS-deficient mice exhibit insulin resistance, including hyperglycemia, hyperinsulinemia, glucose intolerance, de- creased insulin sensitivity, and increased hepatic glucose production. The administration of ectopic IRTKS can ame- liorate the insulin resistance of IRTKS-deficient and diabetic mice. In parallel, the expression level of IRTKS was sig- nificantly decreased in diabetic mouse model. Furthermore, DNA hypermethylation of the IRTKS promoter was also observed in these subjects. We also show that IRTKS, as an adaptor of the insulin receptor （IR）, modulates IR-IRSI- PI3K-AKT signaling via regulating the phosphorylation of IR. These findings add new insights into our understand- ing of insulin signaling and resistance.

The phosphatidylinositol 3-kinase complex I （PI3K complex I） is a crucial regulator of autophagy, which contains Beclin 1 （or ATG6）, ATG14L, VPS34 （or the class III phosphatidylinositol 3-kinase and its adaptor VPS15） and AMBRA1, and controls autophagosome formation. In a paper recently published in Cell Research, Xia et aL report that during nutrient deprivation the ubiquitin E3 ligase RNF2 is recruited to the PI3K complex I, and ubiquitinates AMBRA1 to trigger its degradation and downregulate autophagy.

Control of the activity of the microtubule motor cytoplasmic dynein 1 is essential for its function in intracellular transport. A recent paper by McKenney et al. published in Science shows that activation of processive dynein motility requires the formation of cargo adaptor-dynein-dynactin complexes.

The goal of developing treatments for central nervous system（CNS）injuries is becoming more attainable with the recent identification of various drugs that can repair damaged axons.These discoveries have stemmed from screening efforts,large expression datasets and an improved understanding of the cellular and molecular biology underlying axon growth.It will be important to continue searching for new compounds that can induce axon repair.Here we describe how a family of adaptor proteins called 14-3-3s can be targeted using small molecule drugs to enhance axon outgrowth and regeneration.14-3-3s bind to many functionally diverse client proteins to regulate their functions.We highlight the recent discovery of the axon-growth promoting activity of fusicoccin-A,a fungus-derived small molecule that stabilizes 14-3-3 interactions with their client proteins.Here we discuss how fusicoccin-A could serve as a starting point for the development of drugs to induce CNS repair.

The signaling pathways activated by the B-cell antigen receptor （BCR）play a crucial role in the development, activation, and differentiation of B cells. Among them, the activation ofphospha- tidylinositol 3-kinase （PI3K）/Akt is par- ticularly important.1-5 The recruitment of PI3K to the plasma membrane is necessary for the generation ofphospha- tidyl-inositol-3,4,5-triphosphate, which activates PDK1 （Akt/PKB kinase）; in turn, PDK1 activates Akt （Figure 1）.

Bromodomain containing 2 （Brd2） protein belongs to the Bromodomains and Extra Terminal domain （BET） family of chromatin adaptors characterized by the presence of two N-terminal tandem bromodomains and an exclusive C-terminal extra terminal domain （ET） （Belkina and Denis, 2012; Shi and Vakoc, 2014）. Bromodomains are involved in recognizing acetylated histone tails and other acetylated proteins while the ET domain has been implicated in protein-protein interaction.

Humans are exposed to radiofrequency electromagnetic fields （RFEMF） from various sources （e.g., mobile and cordless phones, base stations, TV and radio transmitters, wifi adapters）. So far, there is no evidence that would indicate that RFEMF exposure is causing adverse health effects with respect to cancer, sleep disorder, headache, etc. Some results of in vitro and in vivo experiments revealed negative effects on male fertility. When looking at those studies in detail, many problems are identified with respect to correct dosimetry and proper experimental design. This field of research is notoriously difficult for various reasons, and experiments should be planned and performed with experts from the respective areas.

In this paper we present a novel GPU-oriented method of creating an inherently continuous triangular mesh for tile-based rendering of regular height fields. The method is based on tiling data-independent semi-regular meshes of non-uniform structure, a technique that is quite different from other mesh tiling approaches. A complete, memory efficient set of mesh patterns is created by an off-line procedure and stored into the graphics adapter＇s memory at runtime. At rendering time, for each tile, one of the precomputed mesh patterns is selected for rendering. The selected mesh pattern fits the required level of details of the tile and ensures seamless connection with other adjacent mesh patterns, like in a game of dominoes. The scalability potential of the proposed method is demonstrated through quadtree hierarchical grouping of tiles. The efficiency is verified by experimental results on height fields for terrain representation, where the method achieves high frame rates and sustained triangle throughput on high resolution viewports with sub-pixel error tolerance. Frame rate sensitivity to real-time modifications of the height field is measured, and it is shown that the method is very tolerant and consequently well tailored for applications dealing with rapidly changeable phenomena represented by height fields.