Project description:Disease emergence occurs within the context of ecological communities, and disease driven declines in host populations can lead to complex direct and indirect ecological effects. Varying effects of a single disease among multiple susceptible hosts could benefit relatively resistant species. Beginning in 2013, an outbreak of sea star wasting disease (SSWD) led to population declines of many sea star species along the west coast of North America. Through field surveys and laboratory experiments, we investigated how and why the relative abundances of two co-occurring sea star species, Evasterias troschelii and Pisaster ochraceus, shifted during the ongoing wasting epidemic in Burrard Inlet, British Columbia, Canada. We hypothesized that Evasterias is competitively inferior to Pisaster but more resistant to SSWD. Thus, we predicted that SSWD-induced declines of Pisaster could mitigate the negative effects of SSWD on Evasterias, as the latter would experience competitive release. We document shifts in sea star abundance from 2008-2017: Pisaster abundance and mean size declined during the outbreak, while Evasterias abundance increased from relatively rare to numerically dominant within the intertidal. When exposed to symptomatic sea stars, Pisaster and Evasterias both showed signs of SSWD, but transmission and susceptibility was lower in Evasterias. Despite diet overlap documented in our field surveys, Evasterias was not outcompeted by Pisaster in laboratory trails conducted with the relatively small Pisaster available after the outbreak. Interference competition with larger Pisaster, or prey exploitation by Pisaster during the summer when Evasterias is primarily subtidal, may explain the rarity of Evasterias prior to Pisaster declines. Our results suggest that indirect effects mediated by competition can mask some of the direct effects of disease outbreaks, and the combination of direct and indirect effects will determine the restructuring of a community after disturbance.
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)
Project description:Trithorax group (TrxG) proteins counteract Polycomb silencing by an as yet uncharacterized mechanism. A well-known member of the TrxG is the histone methyltransferase Absent, Small, or Homeotic discs 1 (ASH1). In Drosophila ASH1 is needed for the maintenance of Hox gene expression throughout development, which is tightly coupled to preservation of cell identity. In order to understand the molecular function of ASH1 in this process, we performed affinity purification of tandem-tagged ASH1 followed by mass spectrometry (AP-MS) and identified FSH, another member of the TrxG as interaction partner. Here we provide genome-wide chromatin maps of both proteins based on ChIP-seq. Our Dataset comprises of 4 ChIP-seq samples using chromatin from S2 cells which was immunoprecipitated, using antibodies against Ash1, FSH-L and FSH-SL.