Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851273 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19761362.fastq.gz | Fastqsanger.gz | |||
| SRR19761363.fastq.gz | Fastqsanger.gz | |||
| SRR19761364.fastq.gz | Fastqsanger.gz | |||
| SRR19761365.fastq.gz | Fastqsanger.gz | |||
| SRR19761366.fastq.gz | Fastqsanger.gz |
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Project description:Oxidative stress caused by ground level ozone is a major contributor to yield loss in a number of important crop plants. Soybean (Glycine max) is especially ozone sensitive, and research into its response to oxidative stress is limited. To better understand the genetic response in soybean to oxidative stress, an RNA-seq analysis of two soybean cultivars was performed comparing an ozone intolerant cultivar and an ozone resistant cultivar after being exposed to ozone. A cursory analysis of the transcriptome data revealed differences between cultivars in the expression levels of genes previously implicated in oxidative stress responses, indicating unique cultivar-specific responses. An examination of the timing of gene responses over the course of ozone exposure showed expression of cuticle wax genes in the intolerant line over all sampled time points, whereas the tolerant line only expressed this pathway in the first time point. The ozone tolerant cultivar has a thicker leaf structure and we believe this lends a passive benefit to the plant which the intolerant cultivar is attempting to supplement via cuticle wax synthesis. These results suggest that differences in genetic responses work in concert with physiological differences to explain differences in ozone tolerance between soybean cultivars.
2016-01-21 | GSE59076 | GEO
Project description:Glycine max cultivar:Fiskeby III Transcriptome or Gene expression
| PRJNA1164167 | ENA
Project description:Glycine max strain:Fiskeby III | cultivar:PI 438471 Genome sequencing
| PRJNA1107527 | ENA
Project description:Tropospheric ozone (O3) is a secondary air pollutant and anthropogenic greenhouse gas. Concentrations of tropospheric O3 have more than doubled since the Industrial Revolution, and are high enough to damage plant productivity. Soybean (Glycine max L. Merr.) is the worldâs most important legume crop and is sensitive to O3. Current ground-level O3 are estimated to reduce global soybean yields by 6% to 16%. In order to understand transcriptional mechanisms of yield loss in soybean, we examined the transcriptome of soybean flower and pod tissues exposed to elevated O3 using RNA-Sequencing.
2015-01-31 | E-MTAB-5226 | biostudies-arrayexpress
Project description:Rice grain yield is predicted to decrease in the future because of an increase in tropospheric ozone concentration. However, the underlying mechanisms are unclear. Here, we investigated the responses to ozone of two rice (Oryza Sativa L.) cultivars, Sasanishiki and Habataki. Sasanishiki showed ozone-induced leaf injury, but no grain yield loss. By contrast, Habataki showed grain yield loss with minimal leaf injury. A QTL associated with grain yield loss caused by ozone was identified in Sasanishiki/Habataki chromosome segment substitution lines and included the ABERRANT PANICLE ORGANIZATION 1 (APO1) gene. The Habataki allele of the APO1 locus in a near-isogenic line also resulted in grain yield loss upon ozone exposure, suggesting APO1 involvement in ozone-induced yield loss. Only a few differences in the APO1 amino acid sequences were detected between the cultivars, but the APO1 transcript level was oppositely regulated by ozone exposure: i.e., it increased in Sasanishiki and decreased in Habataki. Interestingly, the levels of some phytohormones (jasmonic acid, jasmonoyl-L-isoleucine, and abscisic acid) known to be involved in attenuation of ozone-induced leaf injury tended to decrease in Sasanishiki but to increase in Habataki upon ozone exposure. These data indicate that ozone-induced grain yield loss in Habataki is caused by a reduction in the APO1 transcript level through an increase in the levels of phytohormones that reduce leaf damage.
2015-01-31 | GSE65465 | GEO
Project description:Chinese soybean (Glycine max (L.) Merr.) cultivars Rsmv1 and Ssmv1 were used for soybean mosaic virus (SMV) resistance genes screening. The Rsmv1 cultivar was highly-resistant to SMV but the Ssmv1 cultivar was highly-susceptible. We used microarrays to detail the global programme of gene expression underlying SMV inoculation and identified distinct expression genes between Rsmv1 and Ssmv1.
2016-11-23 | GSE90448 | GEO
Project description:Rice grain yield is predicted to decrease in the future because of an increase in tropospheric ozone concentration. However, the underlying mechanisms are unclear. Here, we investigated the responses to ozone of two rice (Oryza Sativa L.) cultivars, Sasanishiki and Habataki. Sasanishiki showed ozone-induced leaf injury, but no grain yield loss. By contrast, Habataki showed grain yield loss with minimal leaf injury. A QTL associated with grain yield loss caused by ozone was identified in Sasanishiki/Habataki chromosome segment substitution lines and included the ABERRANT PANICLE ORGANIZATION 1 (APO1) gene. The Habataki allele of the APO1 locus in a near-isogenic line also resulted in grain yield loss upon ozone exposure, suggesting APO1 involvement in ozone-induced yield loss. Only a few differences in the APO1 amino acid sequences were detected between the cultivars, but the APO1 transcript level was oppositely regulated by ozone exposure: i.e., it increased in Sasanishiki and decreased in Habataki. Interestingly, the levels of some phytohormones (jasmonic acid, jasmonoyl-L-isoleucine, and abscisic acid) known to be involved in attenuation of ozone-induced leaf injury tended to decrease in Sasanishiki but to increase in Habataki upon ozone exposure. These data indicate that ozone-induced grain yield loss in Habataki is caused by a reduction in the APO1 transcript level through an increase in the levels of phytohormones that reduce leaf damage. Ozone induced gene expression in rice inflorescence meristem was measured at 6 month after exposure to dose of 43.7 nL L-1 (ambient air) and 85.7 nL L-1 (2-fold concentration compared to ambient air) (12 hours mean). The two culticars, Sasanishiki and Habataki, were used for each experiment.
2015-01-31 | E-GEOD-65465 | biostudies-arrayexpress
Project description:Ozone is a major air pollutant in highly populated areas. High levels of ambient ozone have been associated with decreased lung function and increased exacerbations of asthma in children and adults. However, the effects of ozone on the newborn’s lung are largely unknown. This study was aimed at profiling the newborn lung response to ozone at the transcriptome level to define the impact of ozone pollutant on the developing postnatal lung. Newborn mice were exposed to ozone or filtered normal air for 3 h. Total RNA was isolated from lung tissues at 6 and 24 h after completion of exposure and was subjected to gene expression analysis using Whole Mouse Genome Gene Expression 4X44K Microarrays (G2519F-014868, Agilent Technologies). Transcriptome analysis of the postnatal lung indicated that 455 genes were down-regulated and 166 genes were up-regulated by at least 1.5 fold at 6 h post-ozone exposure (t-test, p<0.05). At 24 h post exposure, 543 genes were down-regulated and 323 genes were up-regulated in the lungs of ozone-exposed newborn mice, compared to filtered air-exposed newborn mice (t-test, p<0.05). After controlling for false discovery rate, 50 genes were significantly down-regulated and only 4 genes were up-regulated at 24 h post ozone-exposure (q<0.05). Gene ontology enrichment analysis revealed that cell cycle-associated functions including cell division/proliferation, cellular assembly and organization were the predominant pathways negatively regulated by ozone exposure. These findings suggest that elevated ozone pollution may interfere with lung development and growth in the early age.
2014-03-12 | GSE45166 | GEO
Project description:Tolerance to the air pollutant ozone refers to the phenomenon by which pre-exposure to a relatively low concentration confers protection against from lung injury and inflammation caused by a subsequent challenge with high concentration ozone. We investigated whether alveolar macrophages play a central role in this process. First, we established a model of ozone tolerance in which inbred C57BL/6NJ mice were pre-exposed to 0.8 ppm ozone for 4 days then challenged with 2 ppm ozone on day 7, followed by sacrifice and phenotyping on Day 8. As expected, pre-exposure significantly reduced ozone-induced airway injury and inflammation on day 8. To investigate the role of alveolar macrophages, we treated mice with clodronate on day 5, which reduced macrophage number by ~5-fold. Following ozone challenge on day 7, clodronate treated mice exhibited increased injury compared to vehicle treated controls. Cytokines involved in neutrophil chemotaxis such as IL-6, MIP-1b, and KC, were also significantly elevated in clodronate treated mice. Collectively, these data indicate an important role of AMs in this model of tolerance. To identify differences in the phenotype of AMs caused by pre-exposure to ozone, we isolated AMs from ozone pre-exposed mice vs. filtered air controls using flow sorting and performed RNA-seq analysis of these samples. We found that a number of genes and pathways were altered by ozone pre-exposure, most importantly downregulation of pathways involved in toll-like receptor cell signaling, proinflammatory gene expression, and NF-kB mediated gene regulation.
2025-07-18 | GSE248291 | GEO