Wool shedding
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB31930 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3255914_1.fastq.gz | Fastqsanger.gz | |||
| ERR3255914_2.fastq.gz | Fastqsanger.gz | |||
| ERR3255915_1.fastq.gz | Fastqsanger.gz | |||
| ERR3255915_2.fastq.gz | Fastqsanger.gz | |||
| ERR3255916_1.fastq.gz | Fastqsanger.gz |
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Project description:A transcriptome study of a non-shedding fruit Elaeis oleifera palm
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Project description:The aim of this study is to assess the global transcriptome changes during the shedding of the flower, which normally takes around 6 or 7 days. We selected four time points (from day 0 to day 6) and three different tissues within the flower bud; distal, abscission and proximal zones with three biological replicates. RNA extraction, library prep and paired end sequencing was performed. Our special interest is try to describe the changes in the abscission zone and the two adjacent tissues in order to get a whole picture of the shedding process. We performed a de novo assembly by Trinity and detected the transcripts and expression changes across spatial and temporal comparisons.
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Project description:Salmonella species infect many vertebrate species, and pigs colonized with Salmonella enterica serovar Typhimurium (ST) are usually asymptomatic, making detection of these Salmonella-carrier pigs difficult. The variable fecal shedding of this gram-negative bacteria in such pigs is an important cause of foodborne illness and zoonotic disease. To investigate gene pathways and biomarkers associated with the variance in Salmonella shedding following experimental inoculation, we have initiated the first analysis of the whole blood transcriptional response induced by Salmonella. A population of pigs (n=40) was inoculated with ST and the peripheral blood and feces were collected between 2 and 20 days post-inoculation. Two groups of pigs with either low shedding (LS) or persistent shedding (PS) phenotypes were identified. The global transcriptional changes in response to ST inoculation were identified by Affymetrix Genechip?analysis of peripheral blood RNA at day 0 and day 2 post-inoculation.
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Project description:Myocardial infarction (MI) contributes to cardiac mortality and morbidity. After myocardial infarction the innate immune response is pivotal in clearing of tissue debris as well as scar formation, but exaggerated cytokine and chemokine secretion with subsequent leukocyte infiltration also leads to further tissue damage. Post-translational regulation of cytokine / chemokine signaling occurs via ectodomain shedding through a disintegrin and metalloproteases (ADAMs). Here, we address the value of targeting a previously unknown ADAM10 / CX3CL1 axis in the regulation of neutrophil recruitment early after MI. We show that myocardial ADAM10 is distinctly upregulated in biopsies from patients with ischemia-driven cardiomyopathy and correlates with heart failure progression. Intriguingly, upon MI in mice, pharmacological treatment with the ADAM10 inhibitionor GI254023X as well as genetic cardiomycyte-specific ADAM10 deletion improves survival with markedly enhanced heart function and reduced scar size. Mechanistically, this is driven by abolished ADAM10-mediated CX3CL1 ectodomain shedding followed by diminished IL-1β-dependent inflammation, reduced neutrophil bone marrow egress as well as myocardial tissue infiltration. Genetic cardiomycyte-specific ADAM10 deletion confirmes the small-molecule data and leads to improved cardiac function and reduction in inflammatory markers after ischemic myocardial injury. Thus, our data shows a conceptual insight into how acute MI induces chemotactic signaling via ectodomain shedding in cardiomyocytes.
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