Crotalus scutulatus (Mojave rattlesnake) neurotoxic venom
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ABSTRACT:
PROVIDER: PRJNA395100 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6410430_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR6410431_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR6410429_subreads.fastq.gz | Fastqsanger.gz |
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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:Study of rattlesnake functional variation regulating venom genes
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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:When one phenotype is not enough – divergent evolutionary trajectories govern venom variation in a widespread rattlesnake species
| PRJEB29193 | ENA
Project description:Background The phenotypic polymorphism in rattlesnake venoms has been thoroughly documented, showing a dichotomy between haemorrhagic (Type I) and neurotoxic (Type II) venoms. In South America, the Type II phenotype is predominant; however, evidence exists of Type I haemorrhagic venoms in C. d. ruruima, raising questions about the efficacy of the Crotalus antivenom prepared for the Type II phenotype in treating Crotalus Type I snakebite patients, for whom the administration of Bothrops-Crotalus antivenom has been proposed. Methodology/Principal Findings This study characterises the dichotomy of C. d. ruruima venom based on the structure of isoforms differentially expressed in Type I and Type II venoms, the biological activities of each phenotype, and the implications for the clinical management of snakebites in Northern Brazil. Four toxins were differentially expressed in Type I and Type II venoms: two PIII-class SVMPs, which were highly expressed in Type I venoms and associated with proteolytic and haemorrhagic activity, and two PLA2s, corresponding to Crotoxin A and B chains, identified in Type II venoms and associated with increased phospholipase A2, myotoxic activities, and heightened lethality. The structure of Crotoxin chains was well conserved compared to C. d. terrificus crotoxin. However, compared to Bothropasin, the SVMP sequences exhibited several substitutions in functional and immunoreactive regions, resulting in low haemorrhagic activity and slight reactivity/neutralisation by Bothrops antivenom. In opposition, Crotalus antivenom reacted with high antibody titres and neutralised all activities of both venom subtypes, except the low haemorrhagic activity induced by Type I venoms. Conclusions/Significance The efficacy of Bothrops antivenom in incidents involving snakes of the Type I phenotype remains uncertain, and we advocate for an urgent prospective study in Roraima to assess the outcomes and benefits for patients receiving either Bothrops-Crotalus or solely Crotalus antivenoms following rattlesnake bites. Meanwhile, administering Bothrops-Crotalus antivenom could be warranted. However, it is crucial to remain aware of the issues of injecting heterologous Bothrops antibodies with limited efficacy in treating Crotalus snakebite patients.
2025-07-04 | PXD060738 | Pride
Project description:Sequencing venom PLA2 regions from three rattlesnakes
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Project description:The venom color variation of C. d. terrificus (Cdt) is attributed to the presence of the toxin LAAO. However, the driving mechanisms of such variability have not been studied and identified so far. During the venom milking routine at Butantan Institute, we have noticed that most of the venoms of captive Cdt specimens show a yellowish color, while most of the venoms of wild specimens are white. Here we describe a comparative analysis of long-term captive (LTC) and recently wild-caught (RWC) Cdt, focusing on the enzyme LAAO. For the identification of LAAO in individual venoms, four different approaches were employed: evaluation of the enzymatic activity, SDS-PAGE, Western blotting and ELISA. In addition, mass spectrometry analysis was performed using pooled samples. Although some variation among these methodologies was observed, it was clear the significative higher percentage of individual venom samples presenting LAAO in LTC venoms. LAAO was identified in 60-80% LTC specimens and in only 10-12% of RWC specimens. Furthermore, this enzyme accounts for 5.6% of total venom proteins of LTC Cdt pooled venom, while it corresponds to only 0.7% of RWC Cdt pooled venom. These findings strongly suggest that the captive maintenance increases the expression of LAAO in Cdt venom.
2023-10-23 | PXD019730 | Pride
Project description:Both single cell and bulk RNA sequencing was performed on expanding or differentiating snake venom gland organoids (from Aspidelaps Lubricus Cowlesi and Naja Nivea), or tissue (Aspidelaps Lubricus Cowlesi). Bulk RNA sequencing from the snake venom gland, liver and pancreas was performed to construct a de novo transcriptome using Trinity.
2020-02-24 | GSE129581 | GEO