Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNAseq of 6 day old shoots of 6 rice accessions under WL or WL + supplemental FR (far-red) light

ABSTRACT: This experiment was designed to uncover the transcriptomic changes that would occur in rice after 24 h of supplemental FR treatment, in an accession dependant manner. To do so, 6 different varieties of rice (IR64, Nipponbare, Luk Takhar, M Blatec, Mudgo, Sabharaj and Zhenshan) were grown in the greenhouse facilities of the Botanical Gardens, Utrecht University, in The Netherlands, in summer and autumn of 2021. After five days in WL (400 µmol m-2 s-1 of combined sunlight and artificial light), the treatment group was exposed to supplemental FR (500 µmol m-2 s-1 FR, R:FR of 0.2) light for 24 hours. The whole shoot was sampled, with four plants pooled in one sample. The experiment was repeated four times, resulting in 48 samples (6 varieties x 2 treatments x 4 replicates). Same samples were run on two individual lanes.

INSTRUMENT(S): NextSeq 2000

ORGANISM(S): Oryza sativa

SUBMITTER: Andres Romanowski

PROVIDER: E-MTAB-13023 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrated that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade. The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade. The WT seedlings were grown for 19 days under continuous white light condition before experimental treatment with three light conditions. Seedlings were either maintained in white light for 2 h (WL), incubated in the dark condition for 2 h (D), or experienced a pulse irradiation of FR light before incubated in the dark condition for 2 h (FRD). Total RNAs were separately prepared from leaf blades and petioles after each light treatment. Three independent biological replicates were used.

Project description:Non-optimal fetal environments resulting in low birth weight have epidemiologically been associated with a higher risk of adult diseases. In animal models, maternal undernutrition has successfully demonstrated that offspring owed increased risks for adult diseases. In mice, shorten life span was also demonstrated in offspring following maternal undernutrition. In the present study, we treated pregnant mice with 50% food restriction (FR), and performed global gene expression and promotor DNA methylation profiling on the fetal livers. Considering that effects of food restriction is opposite between before and after birth, we further searched genes which are regulated oppositely against adult calorie restriction (CR) and commonly against aging. Among searched genes, trib1 has already been demonstrated to contribute to a risk of cardiovascular disease, hypertriglyceridaemia and insulin resistance. The present result suggests that expression of trib1 is affected by maternal nutrition, and is one of the most responsible genes for developmental origins of metabolic syndrome. In addition, lepr was also down-regulated by maternal FR, suggested a potential role of this gene in induction of obesity and diabetes. Promotor DNA methylation profiling as well as gene expression profiling revealed that glucocorticoid receptor target genes were regulated by maternal FR. This finding supports previous studies that suggest an important role for glucocorticoid in developmental origins of metabolic syndrome. In the immune system, most of the genes related to interferon were down-regulated in their expression with up-regulation of their promoter DNA methylation. The profiling also suggested diminished NF-κB signalling. These results suggested that maternal FR affected development of the immune system. We presented here a list of genes responsible for developmental origins of health and disease, which were regulated oppositely against adult CR, and commonly against aging, and also affected their promotor DNA methylation. The present list hopefully contributes to prediction of risks for non communicable diseases, and also prediction of prenatal environment of nutrition from offspring materials. Here we carried out global gene expression profiling analysis on the fetal mouse liver following maternal 50% FR. Considering that opposite effects of nutrition between the fetus and adult, we further analyzed our fetal array data by comparing with data from their mothers, and array data on the effect of CR and aging in previous reports using adult rodent tissues. In addition, we performed global DNA methylation analysis using mouse promoter microarray, and compared the results with data of the gene expression analysis. Finally, we presented a list of candidate genes responsible for DOHaD.

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RNAseq of 6 day old shoots of 6 rice accessions under WL or WL + supplemental FR (far-red) light

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