Ontology highlight
ABSTRACT:
PROVIDER: PRJNA395341 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5858070_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR5858071_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR5858072_1.fastq.gz | Fastqsanger.gz | |||
| SRR5858072_2.fastq.gz | Fastqsanger.gz | |||
| SRR5858073_1.fastq.gz | Fastqsanger.gz |
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Project description:Identification of the genetic basis of venom variation in three rattlesnake species
| PRJNA395100 | ENA
Project description:Understanding and predicting the relationships between genotype and phenotype is often challenging, largely due to the complex nature of eukaryotic gene regulation. A step towards this goal is to map how phenotypic variation evolves through genomic changes that modify gene regulatory interactions. Using the Prairie Rattlesnake (Crotalus viridis) and related species, we integrate mRNA-seq, proteomic, ATAC-seq and whole genome resequencing data to understand how specific evolutionary modifications to gene regulatory network components produce variation in venom gene expression. Through comparisons within and between species, we find a remarkably high degree of gene expression and regulatory network variation across even a shallow level of evolutionary divergence. We use these data to test hypotheses about the roles of specific trans-factors and cis-regulatory elements, how these roles may vary across venom genes and gene families, and how variation in regulatory systems drive variation in venom phenotypes. Our results illustrate that variation in chromatin and genotype at regulatory elements plays major roles in modulating expression. However, we also find that enhancer deletions, variation in transcription-factor expression, and variation in activity of the insulator protein CTCF also impact downstream venom phenotypes. Our findings provide insight into the diversity and gene-specificity of gene regulatory features and highlight the value of comparative studies to link gene regulatory network variation to phenotypic variation.
2024-07-17 | GSE254420 | GEO
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: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:Study of rattlesnake functional variation regulating venom genes
| PRJNA1061517 | ENA
Project description:Coevolutionary change requires reciprocal selection between interacting species, i.e., that the partner genotypes that are favored in one species depend on the genetic composition of the interacting species. Coevolutionary genetic variation is manifested as genotype ´ genotype (G ´ G) interactions for fitness from interspecific interactions. Although quantitative genetic approaches have revealed abundant evidence for G ´ G interactions in symbioses, the molecular basis of this variation remains unclear. Here we study the molecular basis of G ´ G interactions in a model legume-rhizobium mutualism using gene expression microarrays. We find that, like quantitative traits such as fitness, variation in the symbiotic transcriptome may be partitioned into additive and interactive genetic components. Our results suggest that plant genetic variation is the largest influence on nodule gene expression, and that plant genotype and the plant genotype ´ rhizobium genotype interaction determine global shifts in rhizobium gene expression that in turn feedback to influence plant fitness benefits. Moreover, the transcriptomic variation we uncover implicates regulatory changes in both species as drivers of symbiotic gene expression variation. Our study is the first to partition genetic variation in a symbiotic transcriptome, and illuminates potential molecular routes of coevolutionary change. We assayed gene expression using three biological replicates for each plant genotype × rhizobium genotype combination (4 combinations) for a total of 12 chips.
2012-05-01 | GSE29027 | GEO
Project description:New treatments that circumvent the pitfalls of traditional antivenom therapies are critical to address the problem of snakebite globally. Numerous snake venom toxin inhibitors have shown promising cross-species neutralization of medically significant venom toxins in vivo and in vitro. The development of high-throughput approaches for the screening of such inhibitors could accelerate their identification, testing, and implementation, and thus holds exciting potential for improving the treatments and outcomes of snakebite envenomation worldwide. Energetics-based proteomic approaches, including Thermal Proteome Profiling (TPP) and Proteome Integral Solubility Alteration (PISA), assays represent “deep proteomics” methods for high throughput, proteome-wide identification of drug targets and ligands. In the following study, we apply TPP and PISA methods to characterize the interactions between venom toxin proteoforms in Crotalus atrox (Western Diamondback Rattlesnake) and the snake venom metalloprotease (SVMP) inhibitor marimastat. We investigate its venom proteome-wide effects and characterize its interactions with specific SVMP proteoforms, as well as its potential targeting of non-SVMP venom toxin families. We also compare the performance of PISA thermal window and soluble supernatant with insoluble precipitate using two inhibitor concentrations, providing the first demonstration of the utility of a sensitive high-throughput PISA-based approach to assess the direct targets of small molecule inhibitors for snake venom.
2024-06-22 | PXD046399 | Pride
Project description:Next Generation Sequencing Identification of HBV-MLL4 integration and its molecular basis in Chinese hepatocellular carcinoma
2025-01-24 | E-GEOD-65485 | ExpressionAtlas
Project description:When one phenotype is not enough – divergent evolutionary trajectories govern venom variation in a widespread rattlesnake species
| PRJEB29193 | ENA
Project description:Identification of a complex genetic network involved in Saccharomyces cerevisiae colony morphology
2015-09-28 | E-GEOD-36151 | ExpressionAtlas