Activation and memory of the heatshock response is mediated by Prion-like domains in Arabidopsis [RNA-seq]
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE260655 | GEO | 2025/01/13
REPOSITORIES: GEO
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Project description:The heatshock factors (HSFs) play a crucial role in this process, but the mechanisms by which plants sense heat stress are not well understood. We find that HSFs act in a network, with sensory HSFs having a modular Prion-domain (PrD) structure that confers temperature dependent phase change behaviour.
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Project description:Prions are self-propagating protein aggregates that act as protein-based genetic elements in fungi. Although prevalent in eukaryotes, prions have not been identified in bacteria. Here we demonstrate that a bacterial protein, transcription terminator Rho of Clostridium botulinum (Cb-Rho), can form a prion. Specifically, we identify a candidate prion-forming domain (cPrD) in Cb-Rho and show that it confers amyloidogenicity on Cb-Rho and can functionally replace the PrD of a yeast prion-forming protein. Furthermore, we show that its cPrD enables Cb-Rho to access alternative conformations in bacteria, a soluble form that terminates transcription efficiently and an aggregated, self-propagating prion form that is functionally compromised, causing genome-wide changes in the transcriptome. Thus, Cb-Rho functions as a protein-based genetic element in bacteria, suggesting that the emergence of prions predates the evolutionary split between eukaryotes and bacteria.
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Project description:Temperature is a major environmental variable governing plant growth and development. ELF3 contains a polyglutamine (polyQ) repeat 8–10, embedded within a predicted prion domain (PrD). We find the length of the polyQ repeat correlates with thermal responsiveness. Plants from hotter climates appear to have lost the PrD domain, and these versions of ELF3 are stable at high temperature and lack thermal responsiveness. ELF3 temperature sensitivity is also modulated by the levels of ELF4, indicating that ELF4 can stabilise ELF3 function. This RNA-Seq dataset provides evidence for the hypothetical ELF3 function of temperature sensing .
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Project description:Heatshock (30 to 37 deg C) and Coldshock (37 to 30 deg C) experiment looking at 5, 15, 30, 45 and 60 mins after the temp change in each condition.
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Project description:Selective vulnerability is an enigmatic feature of neurodegenerative diseases (NDs), whereby a widely expressed protein causes lesions in specific cell types and brain regions. Using the RiboTag method in mice, translational responses of five neural subtypes to acquired prion disease (PrD) were measured. Pre-onset and disease onset timepoints were chosen based on longitudinal electroencephalography (EEG) that revealed a gradual increase in theta power between 10- and 18-weeks after prion injection, resembling a clinical feature of human PrD. At disease onset, marked by significantly increased theta power and histopathological lesions, mice had pronounced translatome changes in all five cell types despite appearing normal. Remarkably, at a pre-onset stage, prior to EEG and neuropathological changes, we found that 1) translatomes of astrocytes indicated reduced synthesis of ribosomal and mitochondrial components, 2) glutamatergic neurons showed increased expression of cytoskeletal genes, and 3) GABAergic neurons revealed reduced expression of circadian rhythm genes. These data demonstrate that early translatome responses to neurodegeneration emerge prior to conventional markers of disease and are cell type-specific. Therapeutic strategies may need to target multiple pathways in specific populations of cells, early in disease.
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Project description:Heterogeneous Tg(hsp70-hRASG12V) embryos were obtained by mating the male homozygous transgenic fish to wildtype females. They were raised to 24 hour-post fertilization (hpf) stage and received heatshock at 37°C in waterbath for one hour, and kept in 28.5°C till 30hpf for RNA extraction. Wildtype embryos receiving the same heatshock treatment were used as controls. Each microarray sample was prepared by pooling 50 embryos and biological duplication was used.
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Project description:Specific insoluble protein aggregates are the hallmarks of many neurodegenerative diseases. For example, cytoplasmic aggregates of the RNA-binding protein TDP-43 are observed in 97% of cases of Amyotrophic Lateral Sclerosis (ALS). However, whether the protein aggregates themselves or other forms of the proteins are toxic to cells is still a very open question for many of these diseases. Here we address this question for TDP-43 by systematically mutating the protein and quantifying the effects on cellular toxicity. In a dataset of >50,000 mutations in the intrinsically disordered prion-like domain (PRD), changes in hydrophobicity and aggregation potential are highly predictive of changes in toxicity. Surprisingly, however, increased hydrophobicity and cytoplasmic aggregation reduce toxicity. Mutations have their strongest effects in a central region of the PRD, with variants that increase toxicity promoting the formation of more dynamic liquid-like condensates. Moreover, the genetic interactions in double mutants indicate that specific secondary structures form in this region and have detectable effects on aggregation and toxicity in vivo. Our results demonstrate that deep mutagenesis is a powerful approach for probing the sequence-function relationships of intrinsically disordered proteins, as well as their in vivo structural conformations. Moreover, they reveal that aggregation of TDP-43 is not toxic but actually protects cells, most likely by titrating the protein away from a toxic liquid-like phase.
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Project description:Heterogeneous Tg(hsp70-hRASG12V) embryos were obtained by mating the male homozygous transgenic fish to wildtype females. They were raised to 24 hour-post fertilization (hpf) stage and received heatshock at 37°C in waterbath for one hour, and kept in 28.5°C till 30hpf for RNA extraction. Wildtype embryos receiving the same heatshock treatment were used as controls. Each microarray sample was prepared by pooling 50 embryos and biological duplication was used. The zebrafish has been established as a powerful vertebrate model organism for large-scale genetic screens and chemical screens. Here, we seek to establish that zebrafish embryos can be utilized as an in vivo system to dissect crucial pathways for oncogenesis. A microarray analysis was performed by comparing transcription profile of heterogeneous Tg(hsp70-hRASG12V) embryos with heatshock to wildtype embryos with heatshock. Both groups of embryos received heatshock at 37°C for one hour at 24 hour-post fertilization (hpf) stage, and kept in 28.5°C till 30hpf for RNA extraction. Each microarray sample was prepared by pooling 50 embryos and biological triplicate was used. Ingenuity Pathway Analysis (IPA) was performed using the upregulated lists. “Cancer “ was the top diseases and disorders, with “Developmental disorder” and “Organismal Injury and Abnormalities” as the second and third diseases and disorders, validating that transient heatshock induction of oncogenic RAS in embryos activates major pathways in oncogenesis.
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Project description:Prion diseases are fatal transmissible neurodegenerative conditions of humans and animals that arise through neurotoxicity induced by PrP misfolding. The cellular and molecular mechanisms of prion-induced neurotoxicity remain undefined. Understanding these processes will underpin therapeutic and control strategies for human and animal prion diseases, respectively. Prion diseases are difficult to study in their natural hosts and require the use of tractable animal models. Here we used RNA-Seq-based transcriptome analysis of prion-exposed Drosophila to probe the mechanism of prion-induced neurotoxicity. Adult Drosophila transgenic for pan neuronal expression of ovine PrP targeted to the plasma membrane exhibit a neurotoxic phenotype evidenced by decreased locomotor activity after exposure to ovine prions at the larval stage. Pathway analysis and quantitative PCR of genes differentially expressed in prion-infected Drosophila revealed up-regulation of cell cycle activity and DNA damage response, followed by down-regulation of eIF2 and mTOR signalling. Mitochondrial dysfunction was identified as the principal toxicity pathway in prion-exposed PrP transgenic Drosophila. The transcriptomic changes we observed were specific to PrP targeted to the plasma membrane since these prion-induced gene expression changes were not evident in similarly-treated Drosophila transgenic for cytosolic pan neuronal PrP expression, or in non-transgenic control flies. Collectively, our data indicate that aberrant cell cycle activity, repression of protein synthesis and altered mitochondrial function are key events involved in prion-induced neurotoxicity, and correlate with those identified in mammalian hosts undergoing prion disease. These studies highlight the use of PrP transgenic Drosophila as a genetically well-defined tractable host to study mammalian prion biology.
2020-01-31 | GSE144028 | GEO
Project description:Alteration of growth condition or disruption of gene function are commonly used strategies to study cellular systems. Although widely appreciated that such experiments may result in indirect effects, these frequently remain uncharacterized. Here, genome-wide expression reanalysis of functionally unrelated Saccharyomyces cerevisiae deletion strains reveals a common expression signature. One property shared by these strains is slower growth, with increased presence of the signature in more slowly growing strains. The slow growth signature is highly similar to the environmental stress response, an expression response common to diverse environmental perturbations. Both environmental and genetic perturbations result in growth rate changes. These are accompanied by a change in the distribution of cells over different cell cycle phases. Rather than representing a direct expression response, the slow growth signature is a consequence of the redistribution of cells over different cell cycle phases, primarily characterized by an increase in the G1 population. The findings have implications for any study of perturbation that is accompanied by growth rate changes. Strategies to counter these effects are presented and discussed. In this series, the effects, over time, of heatshock (shifting cells from 30 to 37 C) or the reverse (cold 'shock') are studied.
2014-05-14 | GSE54528 | GEO