Project description:Immature instars of mayflies are important constituents of the food web in aquatic ecosystems (especially in Neotropical regions) and they are among the most susceptible arthropods to pyrethroid insecticides. These insecticides have been recognized as important stressors of freshwater ecosystems, but their cellular effects in aquatic insects have been neglected. Here, we assessed the susceptibility to deltamethrin (a typical type II pyrethroid) as well as the deltamethrin-mediated cytomorphological changes in the central nervous system and midgut of the mayfly Callibaetis radiatus. While the deltamethrin LC50 for 24 h of exposure was of 0.60 (0.46-0.78) ?g of a.i/L, the survival of C. radiatus was significantly reduced in deltamethrin concentrations ? 0.25 ?g a.i/L at 96 h of exposure. Sub-lethal deltamethrin exposure severely affected the cytomorphology of C. radiatus midgut (e.g., muscle layer retraction, cytoplasm vacuolation, nucleus and striated border disorganization) and also induced slight cytomorphological changes in the brain (e.g., presence of pyknotic nuclei) and in the thoracic ganglia (e.g., vacuolation of neurons and presence of pyknotic nuclei) of these insects. However, DNA damage was absent in all of these organs, suggesting that the sublethal cellular stress induced by deltamethrin might disrupt physiological processes (e.g., metabolism or electrical signal transmission) rather than cause cell death (e.g., apoptosis) in C. radiatus. Thus, our findings indicated that deltamethrin actions at cellular levels represent a clear indication of sublethal effects on the C. radiatus survival abilities.
Project description:<p>In annually reoccurring patterns, microalgae form blooms that persist and decline thereby contributing massively to global biogeochemical cycles. The decline of blooms is mainly caused by nutrient limitation and goes ahead with the aging of individual algal cells. Nutrient intake can re-initiate proliferation, but the processes involved are poorly understood. By investigating the bloom-forming diatom Coscinodiscus radiatus, we demonstrate how algae recover after nutrient influx. The rejuvenation physiology of the algae is characterized by metabolomic re-organization and the formation of extracellular vesicles. Regulated pathways mediating aging are centered around the methionine cycle in C. radiatus. Vesicles shuttle reactive oxygen species, oxylipins and other harmful metabolites out of the old cells, thereby re-enabling their proliferation. Metabolic processes involved in aging and vesicle production are modulated by bacteria. Using chemical signaling bacteria can trigger vesicle production thereby releasing organic nutrients for their growth and supporting algal growth as well.</p><p><br></p><p><strong>Metabolomics profiling of FACS purified EVs</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS5401' rel='noopener noreferrer' target='_blank'><strong>MTBLS5401</strong></a>.</p><p><strong>Metabolomics analysis</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS5368' rel='noopener noreferrer' target='_blank'><strong>MTBLS5368</strong></a>.</p>
Project description:<p>In annually reoccurring patterns, microalgae form blooms that persist and decline thereby contributing massively to global biogeochemical cycles. The decline of blooms is mainly caused by nutrient limitation and goes ahead with the aging of individual algal cells. Nutrient intake can re-initiate proliferation, but the processes involved are poorly understood. By investigating the bloom-forming diatom Coscinodiscus radiatus, we demonstrate how algae recover after nutrient influx. The rejuvenation physiology of the algae is characterized by metabolomic re-organization and the formation of extracellular vesicles. Regulated pathways mediating aging are centered around the methionine cycle in C. radiatus. Vesicles shuttle reactive oxygen species, oxylipins and other harmful metabolites out of the old cells, thereby re-enabling their proliferation. Metabolic processes involved in aging and vesicle production are modulated by bacteria. Using chemical signaling bacteria can trigger vesicle production thereby releasing organic nutrients for their growth and supporting algal growth as well.</p><p><br></p><p><strong>Metabolomics analysis</strong> is reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS5368' rel='noopener noreferrer' target='_blank'><strong>MTBLS5368</strong></a>.</p><p><strong>Metabolomics profiling of FACS purified EVs</strong> is reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS5401' rel='noopener noreferrer' target='_blank'><strong>MTBLS5401</strong></a>.</p>
Project description:modENCODE_submission_5986 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. Our 126 strategically selected targets include RNA polymerase II isoforms, dosage-compensation proteins, centromere components, homolog-pairing facilitators, recombination markers, and nuclear-envelope constituents. We will integrate information generated with existing knowledge on the biology of the targets and perform ChIP-seq analysis on mutant and RNAi extracts lacking selected target proteins. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: L3 Larva; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; EXPERIMENTAL FACTORS: Developmental Stage L3 Larva; temp (temperature) 20 degree celsius; Strain N2; Antibody NURF-1 SDQ3525 (target is NURF-1)