# _embedded.samples[].characteristics.description[].text
Fragment from colony 1 taken from control aquarium after nine days.

# _embedded.samples[].characteristics.description[].text
Fragment from colony 3 taken from control aquarium after nine days.

# _embedded.samples[].characteristics.secondary description[].text
512 Bovine Genome Array 10-19-10_(Bovine)

# _embedded.samples[].organization[].Name
Ospedale Maggiore IRCCS - University of Milan

# _embedded.samples[].characteristics.secondary description[].text
502 Bovine Genome Array 10-19-10_(Bovine)

# _embedded.samples[].characteristics.description[].text
Fragment from colony 1 taken from experimental (dark treated) aquarium after nine days.

# _embedded.samples[].characteristics.sample title[].text
newborn (P0) Krt1+/+ epidermis_replicate 3

# _embedded.samples[].characteristics.description[].text
Fragment from colony 3 taken from experimental aquarium at time zero.

# _embedded.samples[].characteristics.description[].text
Fragment from colony 1 taken from control aquarium at time zero.

# _embedded.samples[].characteristics.submission description[].text
Coral bleaching occurs in response to numerous abiotic stressors, the ecologically most relevant of which is hyperthermic stress due to increasing seawater temperatures. Bleaching events can span large geographic areas and are currently a potent threat to coral reefs worldwide. Much effort has been focused on understanding the molecular and cellular events underlying bleaching, and these studies have mainly utilized heat and light stress regimes. In an effort to determine whether different stressors share common bleaching mechanisms, we used cDNA microarrays for the corals Acropora palmata and Montastraea faveolata (containing > 10,000 features) to measure differential gene expression during darkness stress. This is the first coral microarray experiment aimed at darkness stress, and the first for these species to interrogate gene expression at such a large scale. Our results reveal a striking transcriptomic response to darkness in A. palmata involving chaperone and antioxidant up-regulation, growth arrest, and metabolic modifications. As these responses were also measured during thermal stress, our results suggest that different stressors may share common bleaching mechanisms. Furthermore, our results point to ER stress as a critical cellular event involved in darkness-specific (and possibly more general) molecular bleaching mechanisms. On the other hand, we identified a meager transcriptomic response to darkness in M. faveolata, where gene expression differences between host colonies and/or sampling locations were greater than differences between control and stressed fragments. To this end, we discuss the importance of factors related to host genotype, Symbiodinium genotype, and the abiotic environment that influence host gene expression and thereby can hinder an investigator’s ability to measure gene expression during a condition of interest. We employed a reference design where all control and dark-stressed samples were compared to a pooled reference aRNA sample composed of aRNA from all fragments. Since all RNA samples were compared to the reference sample, direct comparisons of gene expression across all time points and conditions can be performed.

# _embedded.samples[].characteristics.submission title[].text
Microarray studies of darkness stress and bleaching in the Caribbean coral Acropora palmata

# _embedded.samples[].characteristics.description[].text
Gene expression analysis of pollen-pistil interactions in Arabidopsis

# _embedded.samples[].characteristics.sample source name[].text
Arabidopsis pistils 3.5 hours after pollination

# _embedded.samples[].organization[].Name
Ospedale Maggiore IRCCS - University of Milan

# _embedded.samples[].characteristics.submission description[].text
Estrogen plays an important role in the regulation of vascular tone and in the pathophysiology of cardiovascular disease. Physiological effects of estrogen are mediated through estrogen receptors alpha (ERalpha) and beta (ERbeta), which are both expressed in vascular smooth muscle and endothelial cells. However, the molecular pathways mediating estrogen effects in blood vessels are not well defined. We have performed gene expression profiling in the mouse aorta to identify comprehensive gene sets the expression of which is regulated by long-term (1 wk) estrogen treatment. The ER subtype dependence of the alterations in gene expression was characterized by parallel gene expression profiling experiments in ERalpha-deficient [ERalpha knockout (ERalphaKO)] and ERbeta-deficient (ERbetaKO) mice. Importantly, these data revealed that ERalpha- and ERbeta-dependent pathways regulate distinct and largely nonoverlapping sets of genes. Whereas ERalpha is essential for most of the estrogen-mediated increase in gene expression in wild-type aortas, ERbeta mediates the large majority of estrogen-mediated decreases in gene expression. Biological functions of the estrogen-regulated genes include extracellular matrix synthesis, in addition to electron transport in the mitochondrion and reactive oxygen species pathways. Of note, the estrogen/ERbeta pathway mediates down-regulation of mRNAs for nuclear-encoded subunits in each of the major complexes of the mitochondrial respiratory chain. Several estrogen-regulated genes also encode transcription factors. Overall, these findings provide a foundation for understanding the molecular basis for estrogen effects on vasculature gene expression. Experiment Overall Design: Six estrogen receptor alpha knockout (ERaKO) and six estrogen receptor beta knockout (ERbKO) mice and ten of their wild-type littermates (all female, 2.5-4.5 months of age) were ovarioectomized. Half the mice from each genotype were implanted with 17beta-estradiol pellets, the other half with placebo pellets. After 7-8 days of estrogen/placebo treatment, aortas were harvested, total RNAs were purified for Affymetrix GeneChip microarray analysis, without pooling. This experiment consists of 6 groups with 3 (ERaKO and ERbKO) or 5 (WT) biological replicates per group, for a total of 22 samples.

# _embedded.samples[].characteristics.submission title[].text
Transcription profiling of mouse vascular tissue from estrogen receptor alpha knockout (ERaKO) and estrogen receptor beta knockout (ERbKO) mice and vs. wild type control, all ovarioectomized treated with 17beta-estradiol pellets vs. placebo

# _embedded.samples[].characteristics.description[].text
All infections were performed with either BCBL-1-derived KSHV or rKSHV.219.

# _embedded.samples[].characteristics.sample characteristics[].text
DTU purified 2 hr chase, equal fraction to t=0

# _embedded.samples[].characteristics.sample source name[].text
DTU purified 2 hr chase, equal fraction to t=0

# _embedded.samples[].characteristics.submission description[].text
Abnormal circadian rhythms, including exposure to light at night, are associated with a higher cancer risk and a poorer prognosis, which may be one of the reasons that the incidence of cancer is increasing in individuals subjected to these stresses. However, the molecular or systemic mechanisms involved in tumor growth under artificial illumination stress conditions have not been identified. In fact, the question of whether artificial illumination stress promotes tumor growth at all is still controversial. To identify the possible mechanisms underlying tumor progression related to circadian rhythms, we set up nude mouse xenograft models. Eight-week-old male nude mice (BALBc nu/nu) were injected with 100ul (1x106 cells) of Hela cells suspension at two separate dorsal sites. Mice were randomly caged (5/cage) and subdivided into L/L (24-hour light cycle; circadian rhythm disruption model) and L/D (12-hour light/dark cycle; normal circadian rhythm model) groups. 11days after injection, we sacrificed one L/L mouse and one L/D mouse, tumors were immediately preserved using liquid nitrogen. Total RNA from tumors were isolated using QIAshredder and RNeasy-Mini kits (Qiagen). We compared the transcriptional profiling of L/L tumor which was derived from 24-hour light cycle (L/L) caging mice with the transcriptional profiling of L/D tumor which was derived from 12-hour light/dark cycle (L/D) caging mice.

# _embedded.samples[].characteristics.submission title[].text
Tumor bearing mice: One group was caged in 24-hour light cycle (L/L), the other group was caged in 12-hour light/dark cycle (L/D)

# _embedded.samples[].characteristics.description[].text
d-CPCTRY_D1, Analysis conducted at Duke University

# _embedded.samples[].characteristics.description[].text
RMA expression value derived from Affymetrix power tools software; core-gene analysis

# _embedded.samples[].organization[].Name
Université Paris Descartes - Hopital Necker-Enfants Malades