Project description:Whole genome microarray data were analyzed to describe the changes in gene transcription profile in human Caco-2 cancer cells under the influence of the extract from iodine-biofortified and non-fortified carrot and lettuce. These iodine-biofortified vegetables can be used as a functional food. Four-condition experiment: iodine-biofortified carrot, non-fortified carrot, iodine-biofortified lettuce, non-fortified lettuce vs. Caco-2 colorectal adenocarcinoma cell line. Three biological replicates and three technical replicates.
Project description:Whole genome microarray data were analyzed to describe the changes in gene transcription profile in human Caco-2 cancer cells under the influence of the extract from iodine-biofortified and non-fortified carrot and lettuce. These iodine-biofortified vegetables can be used as a functional food.
Project description:Perchlorate, which is a ubiquitous and persistent ion, competitively interferes with iodide accumulation in the thyroid, causing iodine deficiency, which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that perchlorate presents very little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of iodine deficient adults and mothers require extra consideration. In an attempt to determine if the effects on gene expression were similar, we compared the thyroidal effects of perchlorate (10 mg/kg) treatment for 14 days in drinking water with those caused by 8 weeks of Iodine-deficiency in rats. The thyroids were collected (N=3 each group) and total mRNA was analyzed using the Affymetrix Rat Genome 230 2.0 GeneChip®. Changes in gene expression were compared with appropriate control groups. We compared the 2-fold gene changes due to I-deficiency with changes due to perchlorate treatment. 189 transcripts were changed by the Iodine-deficient diet and 722 transcripts were changed by the perchlorate treatment. 34% of the transcripts changed by the I-deficient diet were also changed by perchlorate and generally in the same direction. three specific transporter genes, AQP1, NIS, & SLC22A3 were changed by both treatments, indicating that the membrane specific changes were similar. Iodine-deficiency primarily caused changes in retinol and calcium signaling pathways and perchlorate primarily caused changes related to the accumulation of extracellular matrix proteins. This study provides evidence that perchlorate, at least at this dose level, changes more genes and changes different genes compared to iodine deficiency.
Project description:Perchlorate, which is a ubiquitous and persistent ion, competitively interferes with iodide accumulation in the thyroid, causing iodine deficiency, which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that perchlorate presents very little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of iodine deficient adults and mothers require extra consideration. In an attempt to determine if the effects on gene expression were similar, we compared the thyroidal effects of perchlorate (10 mg/kg) treatment for 14 days in drinking water with those caused by 8 weeks of Iodine-deficiency in rats. The thyroids were collected (N=3 each group) and total mRNA was analyzed using the Affymetrix Rat Genome 230 2.0 GeneChip®. Changes in gene expression were compared with appropriate control groups. We compared the 2-fold gene changes due to I-deficiency with changes due to perchlorate treatment. 189 transcripts were changed by the Iodine-deficient diet and 722 transcripts were changed by the perchlorate treatment. 34% of the transcripts changed by the I-deficient diet were also changed by perchlorate and generally in the same direction. three specific transporter genes, AQP1, NIS, & SLC22A3 were changed by both treatments, indicating that the membrane specific changes were similar. Iodine-deficiency primarily caused changes in retinol and calcium signaling pathways and perchlorate primarily caused changes related to the accumulation of extracellular matrix proteins. This study provides evidence that perchlorate, at least at this dose level, changes more genes and changes different genes compared to iodine deficiency. Changes in gene expression due to I-deficiency compared to normal diet for 2 months. Changes in gene expression due to perchlorate in the drinking water compared to normal drinking water for 1 or 14 days. Feeding study in rats.
Project description:Chitin soil amendment is known to improve soil quality, plant growth and plant stress resilience, but the underlying mechanisms are not well understood. In this study, we monitored chitin’s effect on lettuce physiology every two weeks through an eight-week growth period, analyzed the early transcriptional reprogramming and related metabolomic changes of lettuce, in response to crab chitin treatment in peat-based potting soil. In commercial growth conditions, chitin amendment still promoted lettuce growth, increased chlorophyll content, the number of leaves and crop head weight from week six. The flavonoid content in lettuce leaves was altered as well, showing an increase at week two but a decrease from week six. Transcriptomic analysis showed that over 300 genes in lettuce root were significant differentially expressed after chitin soil treatment. Gene Ontology-term (GO) enrichment analysis revealed statistical overrepresentation of GO terms linked to photosynthesis, pigment metabolic process and phenylpropanoid metabolic process. Further analysis of the differentially expressed genes (DEGs) showed that the flavonoid pathway is mostly upregulated whereas the bifurcation of upstream phenylpropanoid pathway towards lignin biosynthesis is mostly downregulated. Metabolomic analysis revealed the upregulation of salicylic acid, chlorogenic acid, ferulic acid, and p-coumaric acid in chitin treated lettuce seedlings. These phenolic compounds mainly influence the phenylpropanoid biosynthesis pathway and may play important roles in plant defense reactions. Our results suggest that chitin soil amendments might activate induced resistance by priming lettuce plants and promote lettuce growth via transcriptional changes.
Project description:In this study, a cross species hybridization (CSH) approach was used to evaluate whole transcriptome changes during carotenoid accumulation in the storage root of carrot (Daucus carota). Carotenoids are isoprenoid compounds providing red, yellow and orange color to plants. Previous gene expression analyses of carotenoid accumulation in non-model plant species have primarily used a candidate gene approach. Since global transcriptome analyses require extensive genome sequence, in the absence of these genomic resources an alternate approach uses platforms developed for model plant species. To assess transcriptome patterns associated with carotenoid pigmentation in carrot storage root, two carrot sibling inbred lines, B8788, true breeding for orange color and B8750, true breeding for white root color, were hybridized to the Medicago Affymetrix GeneChip microarray.
Project description:Lettuce is one of most consumed vegetables globally. This crop is susceptible to abiotic stresses. To understand the molecular mechanisms of stress response in lettuce, global transcriptome analysis was conducted. This analysis revealed distinctive temporal expression patterns among the stress-regulated genes in lettuce plants exposed to abiotic stresses
Project description:In this study, a cross species hybridization (CSH) approach was used to evaluate whole transcriptome changes during carotenoid accumulation in the storage root of carrot (Daucus carota). Carotenoids are isoprenoid compounds providing red, yellow and orange color to plants. Previous gene expression analyses of carotenoid accumulation in non-model plant species have primarily used a candidate gene approach. Since global transcriptome analyses require extensive genome sequence, in the absence of these genomic resources an alternate approach uses platforms developed for model plant species. To assess transcriptome patterns associated with carotenoid pigmentation in carrot storage root, two carrot sibling inbred lines, B8788, true breeding for orange color and B8750, true breeding for white root color, were hybridized to the Medicago Affymetrix GeneChip microarray. Near isogenic recombinant inbred lines B8788 and B8750, derived from a cross between white rooted wild carrot (QAL) and orange-rooted B493 were used for comparative analyzes to minimize background genetic differences. B8788 is true breeding for orange color whereas B8750 is true breeding for white storage root color. Carrots were grown in three pots for each genotype under greenhouse conditions and carrots were selected arbitrarily from these pots for harvest. Roots were harvested at approximately 11 weeks post planting when carotenoid accumulation becomes apparent in the storage root. Storage root tissue from sixteen individual carrot roots was pooled into three one-gram tissue pools of four carrots for each genotype.
Project description:Thyroid autonomy is a frequent cause of thyrotoxicosis in regions with iodine deficiency. Epidemiological data suggest that the prevalence of thyroid autonomy is not only inversely correlated with the ambient iodine supply, but that iodide may also influence the course of pre-existing thyroid autonomy with possibly different effects on thyroid growth and function. Iodine slows TSH effects on thyroid growth stimulation and this effect is more pronounced in thyrocytes with constitutive cAMP activation i.e. in thyroid autonomy. Iodine induced growth alteration in early stage thyroid autonomy is conferred by induction of apoptosis and G2/M arrest. Transcriptome analysis revealed significant modulation of gene networks relevant to cell adhesion, cadherin signalling and ion binding with more pronounced effects in constitutively active FRTL-5 cells compared to normal FRTL-5 cells. The aim was to study iodide-induced changes in global gene expression in an in vitro model of thyroid autonomy. This model makes use of FRTL-5 cells with stable expression of a constitutively activating TSH receptor mutation or wild type TSHR as a control.