Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation

ABSTRACT: Ultraviolet C radiation (UVC) damages the nuclear and mitochondrial genomes; this damage is repaired in the nuclear but not mitochondrial genome. Ethidium bromide (EtBr) inhibits mitochondrial DNA replication. We were interested in the transcriptomic response to exposure to UVC, EtBr, and the combination. The UVC exposure protocol results in a high level of mitochondrial DNA damage, and a low level of nuclear DNA damage (because of repair). We exposed age-matched L1-stage Caenorhabditis elegans to ultraviolet C radiation (UVC ) three times, separated in time by 24 h, in the absence of food. After the third exposure, larvae were placed on K agar plates with OP50 bacterial food. In some cases ethidium bromide was also used. Nematodes were sampled for RNA isolation several times.

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Joel Meyer

PROVIDER: E-GEOD-38997 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Effects of early life exposure to ultraviolet C radiation on mitochondrial DNA content, transcription, ATP production, and oxygen consumption in developing Caenorhabditis elegans.

Leung Maxwell C K MC Rooney John P JP Ryde Ian T IT Bernal Autumn J AJ Bess Amanda S AS Crocker Tracey L TL Ji Alex Q AQ Meyer Joel N JN

BMC pharmacology & toxicology 20130204

<h4>Background</h4>Mitochondrial DNA (mtDNA) is present in multiple copies per cell and undergoes dramatic amplification during development. The impacts of mtDNA damage incurred early in development are not well understood, especially in the case of types of mtDNA damage that are irreparable, such as ultraviolet C radiation (UVC)-induced photodimers.<h4>Methods</h4>We exposed first larval stage nematodes to UVC using a protocol that results in accumulated mtDNA damage but permits nuclear DNA (nD ...[more]

PMID: 23374645

Similar Datasets

Project description:Damage to the mitochondrial genome (mtDNA) severely affects the cell and causes disease. Mutations to mtDNA also accumulate throughout the lifespan of many organisms and may be a proximal cause of aging. There is no effective treatment for ailments caused by mtDNA mutation. Since mitochondrial function and biogenesis are controlled by the nutrient environment of the cell, it is possible that perturbation of conserved, nutrient-sensing pathways may successfully treat mitochondrial disease. Experiments using the tractable eukaryote Saccharomyces cerevisiae allow us to investigate the connection between nutrient-sensing and mitochondrial function. We have focused our current studies on the protein kinase A (PKA) pathway, which controls S. cerevisiae behavior according to glucose availability. We found that reduced PKA signaling can lead, in a background-dependent manner, to improved fitness after mtDNA loss. Specifically, over-expression of the cyclic AMP phosphodiesterase Pde2p, removal of PKA isoform Tpk3p, or ablation of other proteins promoting PKA activity leads to improved proliferation of cells deleted of the mitochondrial genome. Over-expression of Pde2p also suppresses the inviability of several mutants that normally cannot survive mtDNA loss. Moreover, Pde2p over-expression diminishes the nuclear transcriptional response to mtDNA damage, further supporting the idea that glucose sensation is harmful for cells lacking the mitochondrial genome. These findings are heavily dependent upon yeast genetic background. Interestingly, robust import of mitochondrial polytopic membrane proteins may be required in order for cells with no mtDNA to receive the full benefits of PKA reduction. Our findings support the idea that perturbation of nutrient-sensing pathways, and specifically the sensation of glucose, may benefit cells with dysfunctional mitochondria. Four experimental conditions were used: BY4743 (WT) cells containing empty pRS426 vector and containing mtDNA because EtBr was not used, BY4743 (WT) cells containing empty pRS426 vector and lacking mtDNA after 24 hours of treatment with 25 µg/ml ethidium bromide, BY4743 (WT) cells overexpressing TIP41 from plasmid pRS426 and lacking mtDNA after 24 hours of treatment with 25 µg/ml ethidium bromide, and BY4743 (WT) cells overexpressing PDE2 from plasmid pRS426 and lacking mtDNA after 24 hours of treatment with 25 µg/ml ethidium bromide. Two replicates were performed for each sample type.

Dataset Information

Expression data from Caenorhabditis elegans L1-stage larvae exposed to ethidium bromide and/or serial ultraviolet C radiation

Publications

Effects of early life exposure to ultraviolet C radiation on mitochondrial DNA content, transcription, ATP production, and oxygen consumption in developing Caenorhabditis elegans.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets