The Role of Women in the Economy of Kosovo

Inequality in the labor market of Kosovo is persistent; the level of unemployment is very high, with the highest level among women. This paper aims to present the current role of women in the economy of Kosovo; through unpaid or paid work. This paper is based on secondary research, from which patterns about what effects women\u27s current role in the economy of Kosovo were found. Some of these patterns were: \u27motherhood,\u27 gender differences in earnings, education, cultural factor etc. Additionally, this paper is based on the analysis of the results from surveys done to women in high profile jobs and interviews done with individuals who dealt with the role of women in the economy of Kosovo. To conclude with, the purposed of the primary and secondary based research was to identify gender differences in the economy of Kosovo as well as barriers to women\u27s empowerment; in order to give at the end possible recommendations that address women\u27s needs in the economy of Kosovo, specifically in the labor market

Glia Are Required For Sensory Neuron Morphology And Function In Caenorhabditis elegans

The nervous system emerges from the coordinated development of neurons and glia. To better understand the processes that enable nervous system development and function we have studied the sensory organs of Caenorhabditis elegans because their anatomy and function are well-characterized. Specifically, we have focused on two aspects of sensory organs: how do glia interact with neurons to enable proper development and function and how are sensory cilia generated. To uncover any glial roles, we ablated the major glial cell of the amphid sensilla. Embryonic glial ablation did not affect neuronal survival and resulted in sensory neuron dendrites that were far too short, revealing a glial role in anchoring sensory neuron dendrites. To examine post-developmental glial roles, we ablated glia after the amphid sensory organ was fully formed. These glia-ablated animals exhibited profound sensory deficits as determined by behavioral assays, failed to maintain the proper morphology of some modified sensory cilia, and had defects in neuronal uptake of lipophilic dyes. Further, animals lacking glia showed no Ca2+ responses in the ASH sensory neuron after stimulation with a high osmolarity solution. To understand the molecular bases of these glial activities, we characterized a sheath glia expressed gene, fig-1, that encodes a protein with thrombospondin type I domains. FIG-1 likely functions extracellularly, is essential for neuronal dye uptake, and also affects behavior. To characterize the molecular basis of cilia morphogenesis and function, we cloned the che-12 and dyf-11 mutants which have chemotaxis and dye uptake defects. CHE-12 and DYF-11 are conserved ciliary proteins required for maintenance of cilium morphology and function. Furthermore, DYF-11 undergoes intraflagellar transport (IFT) and may function at an early stage of IFT-B particle assembly. Our results suggest that glia are required for multiple aspects of sensory organ function. Moreover, as thrombospondin 1 is a glial-secreted protein required for synapse formation in mice, these results suggest that some of the molecular components underlying glia-neuron interactions in C. elegans might be conserved

Retroauricular Pleomorphic Adenoma Arising from Heterotopic Salivary Gland Tissue

A 38-year-old woman is described who presented with a slowly growing mass on the posterior aspect of the left ear. Excision and histopathologic evaluation revealed a pleomorphic adenoma (PA) originating from heterotopic salivary gland tissue. Many authors have presented cases of PAs originating from ceruminous glands in the external auditory canal or of so-called chondroid syringoma originating from apocrine and eccrine sweat glands. This is the only case in the recent literature of a PA originating from a heterotopic rest of salivary gland tissue in the retroauricular region. The 3 main sources of PAs, their embryologic derivation, and treatment are described

Lipid-Anchored SNAREs Lacking Transmembrane Regions Fully Support Membrane Fusion during Neurotransmitter Release

SummarySynaptic vesicle fusion during neurotransmitter release is mediated by assembly of SNARE- and SM-protein complexes composed of syntaxin-1, SNAP-25, synaptobrevin-2/VAMP2, and Munc18-1. Current models suggest that SNARE-complex assembly catalyzes membrane fusion by pulling the transmembrane regions (TMRs) of SNARE proteins together, thus allowing their TMRs to form a fusion pore. These models are consistent with the requirement for TMRs in viral fusion proteins. However, the role of the SNARE TMRs in synaptic vesicle fusion has not yet been tested physiologically. Here, we examined whether synaptic SNAREs require TMRs for catalysis of synaptic vesicle fusion, which was monitored electrophysiologically at millisecond time resolution. Surprisingly, we find that both lipid-anchored syntaxin-1 and lipid-anchored synaptobrevin-2 lacking TMRs efficiently promoted spontaneous and Ca2+-triggered membrane fusion. Our data suggest that SNARE proteins function during fusion primarily as force generators, consistent with the notion that forcing lipid membranes close together suffices to induce membrane fusion

Gene Activation Using FLP Recombinase in C. elegans

The FLP enzyme catalyzes recombination between specific target sequences in DNA. Here we use FLP to temporally and spatially control gene expression in the nematode C. elegans. Transcription is blocked by the presence of an “off cassette” between the promoter and the coding region of the desired product. The “off cassette” is composed of a transcriptional terminator flanked by FLP recognition targets (FRT). This sequence can be excised by FLP recombinase to bring together the promoter and the coding region. We have introduced two fluorescent reporters into the system: a red reporter for promoter activity prior to FLP expression and a green reporter for expression of the gene of interest after FLP expression. The constructs are designed using the multisite Gateway system, so that promoters and coding regions can be quickly mixed and matched. We demonstrate that heat-shock-driven FLP recombinase adds temporal control on top of tissue specific expression provided by the transgene promoter. In addition, the temporal switch is permanent, rather than acute, as is usually the case for heat-shock driven transgenes. Finally, FLP expression can be driven by a tissue specific promoter to provide expression in a subset of cells that can only be addressed as the intersection of two available promoters. As a test of the system, we have driven the light chain of tetanus toxin, a protease that cleaves the synaptic vesicle protein synaptobrevin. We show that we can use this to inactivate synaptic transmission in all neurons or a subset of neurons in a FLP-dependent manner

SUMOylation of Syntaxin1A regulates presynaptic endocytosis

Neurotransmitter release from the presynaptic terminal is under very precise spatial and temporal control. Following neurotransmitter release, synaptic vesicles are recycled by endocytosis and refilled with neurotransmitter. During the exocytosis event leading to release, SNARE proteins provide most of the mechanical force for membrane fusion. Here, we show one of these proteins, Syntaxin1A, is SUMOylated near its C-terminal transmembrane domain in an activity-dependent manner. Preventing SUMOylation of Syntaxin1A reduces its interaction with other SNARE proteins and disrupts the balance of synaptic vesicle endo/exocytosis, resulting in an increase in endocytosis. These results indicate that SUMOylation regulates the emerging role of Syntaxin1A in vesicle endocytosis, which in turn, modulates neurotransmitter release and synaptic function

Author response

We recently reported that the C2AB portion of Synaptotagmin 1 (Syt1) could self-assemble into Ca(2+)-sensitive ring-like oligomers on membranes, which could potentially regulate neurotransmitter release. Here we report that analogous ring-like oligomers assemble from the C2AB domains of other Syt isoforms (Syt2, Syt7, Syt9) as well as related C2 domain containing protein, Doc2B and extended Synaptotagmins (E-Syts). Evidently, circular oligomerization is a general and conserved structural aspect of many C2 domain proteins, including Synaptotagmins. Further, using electron microscopy combined with targeted mutations, we show that under physiologically relevant conditions, both the Syt1 ring assembly and its rapid disruption by Ca(2+) involve the well-established functional surfaces on the C2B domain that are important for synaptic transmission. Our data suggests that ring formation may be triggered at an early step in synaptic vesicle docking and positions Syt1 to synchronize neurotransmitter release to Ca(2+) influx. DOI: http://dx.doi.org/10.7554/eLife.17262.00