Cymodocea nodosa response to simulated CO2-driven ocean acidification
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 1000
ORGANISM(S): Cymodocea nodosa
SUBMITTER: Francesco Musacchia
PROVIDER: E-MTAB-4232 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional reprogramming and stimulation of leaf respiration by elevated CO2 concentration is diminished, but not eliminated, under limiting nitrogen supply. Arabidopsis plants were grown in either ambient (370 ppm) or elevated (750 ppm) CO2 with either ample N supply or limiting N supply. Leaf tissue was harvested from youngest most fully expanded leaves 35 days after plant germination at either midday or midnight.
2013-10-15 | E-GEOD-50966 | biostudies-arrayexpress
Project description:Plant respiration responses to elevated growth [CO2] are key uncertainties in predicting future crop and ecosystem function. In particular, the effects of elevated growth [CO2] on respiration over leaf development are poorly understood. This study tested the prediction that, due to greater whole-plant photoassimilate availability and growth, elevated [CO2] induces transcriptional reprogramming and a stimulation of nighttime respiration in leaf primordia, expanding leaves, and mature leaves of Arabidopsis thaliana. In primordia, elevated [CO2] altered transcript abundance, but not for genes encoding respiratory proteins. In expanding leaves, elevated [CO2] induced greater glucose content and transcript abundance for some respiratory genes, but did not alter respiratory CO2 efflux. In mature leaves, elevated [CO2] led to greater glucose, sucrose and starch content, plus greater transcript abundance for many components of the respiratory pathway, and greater respiratory CO2 efflux. Therefore, growth at elevated [CO2] stimulated dark respiration only after leaves transitioned from carbon sinks into carbon sources. This coincided with greater photoassimilate production by mature leaves under elevated [CO2] and peak respiratory transcriptional responses. It remains to be determined if biochemical and transcriptional responses to elevated [CO2] in primordial and expanding leaves are essential prerequisites for subsequent alterations of respiratory metabolism in mature leaves. Arabidopsis plants were grown in either ambient (370 ppm) or elevated (750 ppm) CO2. Leaf number 10 was harvested when it was a primordia, expanding, or mature in each of the CO2 treatments.
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2016-06-10 | E-GEOD-80158 | biostudies-arrayexpress
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2012-03-07 | E-GEOD-27985 | biostudies-arrayexpress
Project description:Perfluorooctanoic acid (PFOA) is a potent hepatocarcinogen and peroxisome proliferator (PP) in rodents. Humans are not susceptible to peroxisome proliferation and are thought to be refractory to carcinogenesis by PFOA and other PPs. However, previous studies with rainbow trout have shown that they are also insensitive to peroxisome proliferation by the PP, dehydroepiandrosterone (DHEA), but are still susceptible to enhanced hepatocarcinogenesis after chronic exposure. In this study, we determined whether PFOA is also a tumor promotor in trout and then examined hepatic gene expression profiles to further investigate possible mechanisms of action. Trout were initiated as fry to the hepatocarcinogen, aflatoxin B1, and then fed 200-1800 ppm PFOA in the diet for 30 weeks. Two structurally diverse PPs, clofibrate (CLOF) and DHEA, were included for comparison. Hepatic gene expression profiles were subsequently examined in animals exposed to similar doses of PFOA, DHEA and CLOF along with 5 ppm 17β-estradiol (E2; a known tumor promotor) in the diet. PFOA (1800 ppm) and DHEA treatments resulted in enhanced liver tumor incidence and multiplicity while CLOF showed no effect. Carcinogenesis seemed independent of peroxisome proliferation as no induction of peroxisomal β-oxidation and catalase activity were observed. Alternately, plasma VTG was elevated in fish fed PFOA and DHEA suggesting that estrogenic mechanisms may play a role. Both tumor promotors, PFOA and DHEA, resulted in strong correlation of transcriptional profiles with E2 by Pearson correlation (R=0.81 and 0.78, respectively). In comparison, CLOF regulated no genes in common with E2. Overall, these data suggest that the tumor promoting activities of DHEA and PFOA in trout are independent of peroxisome proliferation and may involve estrogenic mechanisms. Juvenile trout, 12-18 months old, were fed experimental diets containing 500 or 1800 ppm PFOA, 1800 ppm CLOF, 750 ppm DHEA, 5 ppm E2 or 0.15 % dimethyl sulfoxide vehicle control for 14 days. Liver samples were collected for microarray analysis. Hybridizations were performed using standard reference design with dye-swapping. For each sample, equal amounts of RNA (µg) were pooled from five fish per tank for every treatment (n=3 biological replicates per treatment). cDNA from two of the three biological replicates was dye-swapped and hybridized to two slides as technical replicates (5 arrays per treatment).
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