Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1211663 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32027824_1.fastq.gz | Fastqsanger.gz | |||
| SRR32027824_2.fastq.gz | Fastqsanger.gz | |||
| SRR32027825_1.fastq.gz | Fastqsanger.gz | |||
| SRR32027825_2.fastq.gz | Fastqsanger.gz | |||
| SRR32027826_1.fastq.gz | Fastqsanger.gz |
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Project description:Spiders have distinct capture prey behaviors selected along Araneae´s evolutive history, but mainly based on the use of venom for prey paralysis. Uloboridae spiders lost the venom glands secondarily in evolution. Due to that they extensively wrap prey with silk to paralyze and begin digestion. During the extra-oral digestion, the digestive fluid very efficiently performs the liquefaction of both the prey and the AcSp2 spidroins from the web fibers. Despite the efficiency of this process, the cocktail of enzymes involved in digestion in Uloboridae spiders is unknown. In this study, we evaluated the protein content in the midgut of Uloborus sp. using enzymatic, proteomic, and phylogenetic analysis approaches. Hydrolases as peptidases (endo and exopeptidases: cysteine, serine and metallopeptidases), carbohydrases (alpha-amylase, chitinase, alpha-mannosidase), and lipases were biochemically assayed; 50 proteins, annotated as enzymes, structural proteins, and toxins, were identified. This is the first characterization of the molecules involved in the digestive process and the midgut protein content of a nonvenomous spider.
2023-03-11 | PXD037345 | Pride
Project description:We generated ATAC-seq data for pre- and post-extraction venom gland samples and H3K4me3, H3K27ac, and CTCF ChIP-seq from post-extraction venom gland samples from the Prairie Rattlesnake to investigate patterns of chromatin accessibility, transcription factor binding, and insulation during venom production, and to identify open promoters and active enhancer regions.
2022-04-07 | GSE169217 | GEO
Project description:Drosophila melanogaster lost, lost, is differentially expressed in 11 experiment(s);
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Project description:Background The generalist dipteran pupal parasitoid Nasonia vitripennis injects 79 venom peptides into the host before egg laying. This venom induces several important changes in the host, including developmental arrest, immunosuppression, and alterations to normal metabolism. It is hoped that diverse and potent bioactivities of N. vitripennis venom provide an opportunity for the design of novel acting drugs. However, currently very little is known about the individual functions of N. vitripennis venom peptides and less than half can be bioinformatically annotated. The paucity of annotation information complicates the design of studies that seek to better understand the potential mechanisms underlying the envenomation response. Although the RNA interference system of N. vitripennis provides an opportunity to functionally characterise venom encoding genes, with 79 candidates this represents a daunting task. For this reason we were interested in determining the expression levels of venom encoding genes in the venom gland, such that this information could be used to rank candidate venoms. To do this we carried out deep sequencing of the transcriptome of the venom gland and neighbouring ovary tissue and used RNA-seq to measure expression from the 79 venom encoding genes. The generation of a specific venom gland transcriptome dataset also provides further opportunities to investigate novel features of this highly specialised organ. Results High throughput sequencing and RNA-seq revealed that the highest expressed venom encoding gene in the venom gland was a serine protease called Nasvi2EG007167, which has previously been implicated in the apoptotic activity of N. vitripennis venom. As expected the RNA-seq confirmed that the N. vitripennis venom encoding genes are almost exclusively expressed in the venom gland relative to the neighbouring ovary tissue. Novel peptides appear to perform key roles in N. vitripennis venom function as only four of the highest 15 expressed venom encoding genes are bioinformatically annotationed. The high throughput sequencing data also provided evidence for the existence of an additional 471 novel genes in the Nasonia genome that are expressed in the venom gland and ovary. Finally, metagenomic analysis of venom gland transcripts identified viral transcripts that may play an important part in the N. vitripennis venom function. Conclusions The expression level information provided here for the 79 venom encoding genes provides an unbiased dataset that can be used by the N. vitripennis community to identify high value candidates for further functional characterisation. These candidates represent bioactive peptides that have value in drug development pipelines.
2016-12-31 | GSE76257 | GEO
Project description:The Mojave rattlesnake (Crotalus scutulatus scutulatus) is classified as the “highest medically important” snake in the risk categories in the United States. Although responsible for fewer snakebite envenomations and deaths compared to other species, Mojave rattlesnake venom is poorly characterized and shows significant geographical variability. The venom of Type A animals primarily contains the β-neurotoxin referred to as Mojave Toxin (MTX), which is responsible for the neurotoxic effects that make bites from this snake particularly feared. Previous studies have shown that β-neurotoxin from different snake species produced similar but complex effects by mechanisms that are not fully understood. We performed a genome-wide transcriptomic analysis of the neurocellular response to Mojave Type A rattlesnake venom using induced pluripotent stem cell (iPSC) -derived human neural stem cells (NSCs) to unveil the molecular mechanisms underlying the damage caused by this snake’s envenomation. Our results suggest that snake venom metalloproteases (svMPs), although have a limited repertoire in type A animal venom, facilitate venom spread by digesting tissue's extracellular matrix. The MTX, which is composed of heterodimers of basic and acidic phospholipase A2 (PLA2) and is the dominant constituent of this venom, co-opts the host arachidonic acid and Ca2+ second messenger mechanisms in a dose- and time-dependent escalating venom damage. The release of arachidonic acid and the rapid increase in intracellular Ca2+ caused by the PLA2 activity of MTX triggers multiple signaling cascades. The activation of MAPKs and NF-κB regulated proinflammatory cascades were the top enriched pathways in the shorter 4-hour NSC response to venom challenge and suggest a significant role of PKC-δ in the activation of MAPKs. The rapid increase in intercellular Ca2+ and resulting cellular depolarization plausibly have a role in neurotransmitter overload in the cholinergic and glutamatergic excitatory synapses and MTX-induced presynaptic blockade of nerve signals. The expression of the acetylcholinesterase gene (ACHE), which degrades acetylcholine, and the downregulation of GRIK1 and GRIK3 genes, which encode KA-iGluRs proteins suggest a cellular response to neurotransmitter overload in the excitatory synapses. Our results also show that the MTX/svPLA2 mediated dysregulation of Ca2+ homeostasis, particularly depletion from the endoplasmic reticulum (ER), causes ER stress and upregulation of unfolded protein response (UPR). The UPR and the oxidative stress caused by ROS generated in CYP1A1-mediated hydroxylation of arachidonic acid, contribute to mitochondrial membrane permeabilization. The activation of UPR, mitochondrial toxicity, and oxidative stress, constitute the degenerative phase of the venom challenge in NSCs and synergistically contribute to apoptotic and ferroptotic programmed cell death.
2025-04-02 | GSE287744 | GEO
Project description:Mucuna pruriens extract MPE pretreatment may have a direct protective effect on heart (other than immunological neutralization of the venom neurotoxin and phospholipase A2 by the anti-MPE antibodies) that renders the heart more resistant to the toxic action of the venom The direct protective effect probably involves functional changes to the cardiac tissue that enable the heart to resist the reduction of contractility and rate induced by the cobra venom.To explore the possibility of the direct action of MPE pretreatment on heart and to understand the molecular events involved in the protection of MPE pretreatment against the lethal action of Naja sputatrix venom, gene expression studies were carried out using microarray analysis. Rats were divided into four groups (n=6): negative control (abbreviated as ‘negative’ group), MPE pretreated group (abbreviated as ‘MPE’ group), N. sputatrix venom-challenge group (abbreviated as ‘NS’ group) and N. sputatrix venom-challenge to MPE pretreated animals group (abbreviated as ‘MPE-NS’ group). In the ‘MPE’ group, rats were injected with MPE at a dose of 21 mg/kg (i.p.), on day 0, 7 and 14, and sacrificed on day 21. In the ‘negative’ group (the untreated, control group), rats were injected with saline of the same volume and sacrificed also on day 21. Hearts were then harvested immediately. In the N. sputatrix venom-challenge group (‘NS’ group), untreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom whereas in the venom challenge to MPE pretreated animals group (the ‘MPE-NS’ group), MPE pretreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom, both on day 21. For the ‘NS’ and ‘MPE-NS’ group, the rats were observed for 24 h after venom challenged and hearts were harvested as soon as death occurred or 24 h after the venom injection, whichever occurred first.
2014-12-22 | E-GEOD-46610 | biostudies-arrayexpress