PHOTOTROPIN 1 and 2 regulate photosynthesis and UV-induced oxidative stress and cell death
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA601526 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10901416.fastq.gz | Fastqsanger.gz | |||
| SRR10901417.fastq.gz | Fastqsanger.gz | |||
| SRR10901418.fastq.gz | Fastqsanger.gz | |||
| SRR10901419.fastq.gz | Fastqsanger.gz | |||
| SRR10901420.fastq.gz | Fastqsanger.gz |
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Project description:Phototropins are plasma membrane‐associated photoreceptors of blue light. Arabidopsis thaliana genome has two genes, PHOT1 and PHOT2, encoding two phototropins that mediate phototropism, chloroplast positioning and stomatal opening. They are well characterized in terms of photomorphogenetic processes, but so far little was known about their involvement in photosynthesis and response to stress factors triggering oxidative stress and cell death. This work fills the gap in our understanding of PHOT1 and PHOT2 involvement in these processes. We used UV-C treatment to promote oxidative stress and cell death in Arabidopsis thaliana wild-type (Col-0 gl1), phot1, phot2 and phot1/phot2 mutants. Using RNAseq we identified genes differentially expressed in phot mutants, in comparison to the wild-type, in both non-stress conditions and after UV-C stress.
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Project description:We have published results demonstrating that UV-C induces apoptotic-like changes in Arabidopsis (Danon and Gallois FEBS lett (1998) 437: 131-136). The Programmed Cell Death "phenotype" of nucleus shape, DNA laddering caspase-like activity is similar to what has been described in other plant PCD. This demonstrates that UV-C is an appropriate and controllable trigger to study PCD in plants. Using selected mutants and a set of chosen conditions we are aiming at identifying genes that are part of the PCD pathways in plants and filter out the general stress response. We are asking for a medium size experiment knowing that additional microarray analysis are likely to be required to refine the results obtained. We are currently awaiting the results of Affymetrix RNAs hybridisation of PCD-induced wild type that will define the appropriate single time point of the proposed analysis. The rationale is to vary treatments in order to distinguish changes in gene transcription arising from general cellular stress responses to the trigger used from those specific to PCD: 1. We will use wild-type Arabidopsis seedlings as a negative control to provide the basal gene expression pattern. 2. A dose of UV-C radiation of 1KJ/m2. We will irradiate wild type with this non PCD-inducing dose of UV-C radiation to identify sets of genes that respond to UV-induced damage but whose expression is not linked to cell death. 3. A dose of UV-C radiation of 50 KJ/m2. We will irradiate wild type with a PCD-inducing dose of UV-C radiation to identify sets of genes that respond to UV-induced damage and cell death. 4. We have shown that the cell death induced by UV is light dependant, the control, sub-inducing dose and inducing dose treatments will be repeated and the plants kept in the dark until RNA sampling. In those conditions there is no PCD.
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Project description:Plants use sunlight as a source of energy for photosynthesis but also as an important environmental cue to regulate growth, development and light acclimation. Wavelengths in the UV-B (280-315 nm) and UV-A/blue (315-500 nm) regions of the spectrum are perceived by UV RESISTANCE LOCUS 8 (UVR8) and cryptochromes (CRY1 and CRY2), respectively. Despite recent advances in our understanding of how these photoreceptors promote photomorphogenesis, very little is known about the molecular mechanisms regulated by UVR8 and CRYs in sunlight exposed plants. Here, a factorial experiment was designed to assess the roles of UVR8 and CRYs in regulating transcriptome wide changes, hormone accumulation, and growth competence of Arabidopsis thaliana plants exposed to solar UV-B, UV-A, and blue radiation.
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Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94618 | GEO
Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94615 | GEO
Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94620 | GEO
Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94621 | GEO
Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94616 | GEO
Project description:Abstract — Insensitive munitions (IMs) improve soldier safety by decreasing sympathetic detonation during training and use in theatre. The environmental effects of IM constituents such as nitroguanidine (NQ) and IM mixture formulations such as IMX-101 remain largely unknown. In the present study, we investigated the acute (96h) toxicity of NQ and IMX-101 to zebrafish larvae, both in the parent IMs and in IMs irradiated with environmentally-relevant levels of ultraviolet (UV) energy. Zebrafish were exposed to control and ten concentrations of NQ ranging from 1 to 732 mg/L (measured concentrations) or seven concentrations of IMX-101 ranging from 2 to 122 mg/L (measured concentrations) of the parent material or material that had been UV-irradiated (UV-treated) at the equivalent of 24 hours of sunlight. The UV-treatment increased the toxicity of NQ by 17-fold, indicated by a decreased LC50 from 1323 mg/L (parent compound) to 77.2 mg/L. Similarly, UV-treatment increased the toxicity of IMX-101 by nearly two fold (LC50 decreased from 131.3 to 67.6 mg/L). Molecular responses to parent and UV-treated IMs were assessed using global transcript expression assays. Both gene set enrichment analysis (GSEA) and differential transcript expression analysis coupled with pathway and annotation cluster enrichment were conducted to provide functional interpretations of expression results and hypothetical modes of toxicity. The parent NQ exposure caused significant enrichment of functions related to immune responses and proteasome-mediated protein metabolism occurring primarily at low, sublethal exposure levels (5.5 and 45.6 mg/L). Enriched functions in the IMX-101 exposure were indicative of increased xenobiotic metabolism, oxidative stress mitigation, protein degradation, and anti-inflammatory responses, each of which displayed predominantly positive concentration-response relationships. UV-treated NQ had a fundamentally different transcriptomic expression profile relative to parent NQ where positive concentration-response relationships were observed for genes involved in oxidative-stress mitigation pathways whereby we hypothesize that the increased toxicity of UV-treated NQ resulted from increased oxidative stress. This hypothesis was supported by transcriptomic responses indicative of oxidative-stress responses involved in zebrafish development, especially neurological development of visual systems and the brain. Transcriptomic profiles were similar between UV-treated versus parent IMX-101 exposures, however, more significant and diverse enrichment as well as greater magnitudes of differential expression for oxidative stress responses were observed in UV-treated IMX-101 exposures. Further, transcriptomics indicated potential for cytokine signaling suppression providing potential connections between oxidative stress and anti-inflammatory responses. Given these result, we hypothesize that the increased toxicity of UV-irradiated NQ and the IMX-101 mixture result from breakdown products with increased potential to elicit oxidative stress.
2017-08-25 | GSE94614 | GEO
Project description:Ultraviolet (UV) light induces the formation of bulky UV photoproducts in the genome that interfere with DNA replication and transcription. It is well-established how human cells repair UV light-induced DNA lesions, however the signaling pathways and mechanisms that regulate transcription after exposure to UV light are poorly understood. Here, we provide a systematic view on dynamic protein phosphorylation patterns induced by UV light and uncover the dependencies of phosphorylation events on canonical DNA damage kinases and the p38 MAP kinase pathway. Notably, we demonstrate that p38 and its downstream effector kinase MK2 are responsible for one quarter of protein phosphorylation induced by UV light. We identify RNA binding proteins as primary targets and 14-3-3 family proteins as direct readers of UV light-induced, p38-MK2-dependent phosphorylation. Importantly, we demonstrate that UV light triggers rapid and dynamic phosphorylation of the negative elongation factor (NELF) complex subunit NELFE on serine 115 that mediates its binding to 14-3-3. NELFE interaction with 14-3-3 stabilizes NELFE and RNA pol II interaction on the chromatin and inhibits transcriptional elongation, thereby promoting cell survival after UV light.
2019-11-24 | GSE90554 | GEO