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ABSTRACT:
PROVIDER: PRJNA1188357 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Investigate genes associated with Phn7.1, a major QTL influencing partial resistance to the soil-borne pathogen Phytophthora nicotianae in tobacco. Methods: Resistant and susceptible tobacco near isogenic lines with and without Phn7.1 QTL were subjected to the inoculation with Phytophthora nicotianae suspension and suspension buffer without pathogen as control followed by sample collection at 42 hour past inoculation for RNA-seq analysis. Results: Revealed gene expression profiles associated disease resistance and susceptiblilty.
2021-09-14 | GSE168854 | GEO
Project description:For decades the tobacco plant has served as a model organism in plant biology to answer fundamental biological questions in the areas of plant development, physiology, and genetics. Due to the lack of sufficient coverage of genomic sequences, however, none of the expressed sequence tag (EST)-based chips developed to date cover gene expression from the whole genome. The availability of Tobacco Genome Initiative (TGI) sequences provides a useful resource to build a whole genome exon array, even if the assembled sequences are highly fragmented. Here, the design of a Tobacco Exon Array is reported and an application to improve the understanding of genes regulated by cadmium (Cd) in tobacco is described. From the analysis and annotation of the 1,271,256 Nicotiana tabacum fasta and quality files from methyl filtered genomic survey sequences (GSS) obtained from the TGI and ~56,000 ESTs available in public databases, an exon array with 272,342 probesets was designed (four probes per exon) and tested on two selected tobacco varieties. Two tobacco varieties out of 45 accumulating low and high cadmium in leaf were identified based on the GGE biplot analysis, which is analysis of the genotype main effect (G) plus analysis of the genotype by environment interaction (GE) of eight field trials (four fields over two years) showing reproducibility across the trials. The selected varieties were grown under greenhouse conditions in two different soils and subjected to exon array analyses using root and leaf tissue to understand the genetic make-up of the Cd accumulation. An Affymetrix Exon Array was developed to cover a large (~90%) proportion of the tobacco gene space. The Tobacco Exon Array will be available for research use through the Affymetrix array catalogue. As a proof of the exon array usability, we have demonstrated that the Tobacco Exon Array is a valuable tool for studying Cd accumulation in tobacco leaves. Data from field and greenhouse experiments supported by gene expression studies strongly suggested that the difference in leaf Cd accumulation between the two specific tobacco cultivars is dependent solely on genetic factors and genetic variability rather than on the environment. 22 samples were used with 3 different experimental factors: [1] 2 different tissues (leaves and roots/lateral), [2] 2 different mutations (V5 and V21), and [3] 2 different stimuli (Soil 1 and Soil 2). 2-3 biological replicates were used. One sample did not pass QC and is not included in this submission.
2012-11-16 | E-GEOD-42319 | biostudies-arrayexpress
Project description:Tobacco rhizosphere soil Genome sequencing
| PRJNA729881 | ENA
Project description:Tobacco is mainly consumed in two different forms (smoking and chewing) that vary in their composition and methods of intake. Despite being the leading cause of oral cancer, the molecular mechanisms resulting in malignancy upon tobacco exposure are yet to be fully elucidated. We therefore sought to compare the molecular alterations in oral keratinocytes exposed to smoke and chewing tobacco. OKF6/TERT1 cells were exposed to cigarette smoke condensate or chewing tobacco for progressively increasing durations (2, 4, 6 and 8 months). We employed a TMT-based quantitative proteomics approach to investigate the adverse effects of chronic cigarette smoke or chewing tobacco exposure in oral keratinocytes. LC/MS3 analysis resulted in the quantification of 5,342 proteins and 2,821 proteins in cigarette smoke and chewing tobacco exposed cells, respectively. Upstream regulator analysis indicates the involvement of distinct regulators in CSC exposed cells compared to STE exposed cells. In addition, exome sequencing revealed discrete genetic alterations in cells exposed to each insult. Current analysis defines a clear distinction in the molecular dysregulation in oral cells in response to different tobacco-based insults. Some of the proteins dysregulated in cigarette smoke or chewing tobacco exposed cells may serve as potential early detection biomarkers which could aid in stratification of patients based on tobacco usage history.
2019-11-08 | PXD007127 | Pride
Project description:Tobacco in its smoke and smokeless form are major risk factors for ESCC (esophageal squamous cell carcinoma). However, molecular alterations associated with smokeless tobacco exposure are poorly understood. In the Indian subcontinent, tobacco is predominantly consumed in chewing form. An understanding of molecular alterations associated with chewing tobacco exposure is vital for identifying molecular markers and potential targets. We developed an in-vitro cellular model by exposing non-transformed esophageal epithelial cells to chewing tobacco over eight month period. Chronic exposure to chewing tobacco led to increase in cell proliferation, invasive ability and anchorage independent growth indicating cell transformation. Molecular alterations associated with chewing tobacco exposure were characterized by carrying out exome sequencing and quantitative proteomic profiling of parental cells and chewing tobacco exposed cells. Quantitative proteomic analysis revealed that established cancer stem cell markers are elevated in tobacco treated cells. Decreased expression of enzymes associated with the glycolytic pathway and increased expression of a large number of mitochondrially localized proteins involved in the electron transport chain as well as enzymes of TCA cycle were also identified. Electron micrographs revealed increase in number and size of mitochondria. Based on these observations, we hypothesise that chronic treatment of esophageal epithelial cells with tobacco leads to a cancer stem cell-like phenotype. These cells also show characteristic OXPHOS phenotype which can be potentially targeted as a therapeutic strategy.
2019-11-11 | PXD013396 | Pride
Project description:The degree of yellowing in tobacco leaves is an important indicator for determining the maturity and harvesting time of tobacco leaves. Reduction in chlorophyll is of utility for promoting the concentrated maturation of tobacco leaves and achieving mechanised harvesting and mining, and utilising tobacco yellow leaf regulatory genes is of great significance for the selection and breeding of tobacco varieties suitable for mechanised harvesting and the resolution of the molecular mechanisms controlling leaf colouration. In this study, the phenotypes of the yellow-leaf K326 and K326 varieties were analysed, and it was observed that the yellow-leaf K326 variety exhibited a distinct yellow leaf phenotype with a significant reduction in chlorophyll content. Subsequently, using a combination of BSA-seq, transcriptomic sequencing (RNA-seq), and proteomic sequencing approaches, we identified the candidate gene Nitab4.5_0008674g0010 that encodes dihydroneopterin aldolase as a factor associated with tobacco leaf yellowing. Finally, by measuring the folate content in K326 and Huangye K326, the folate content in Huangye K326 was observed to be significantly lower than that in K326, thus indicating that folate synthesis plays a crucial role in phenotypic changes in tobacco yellow leaves. This study is the first to use BSA-seq combined with RNA-seq and proteomic sequencing to identify candidate genes in tobacco yellow leaves. The results provide a theoretical basis for the analysis of the mechanism of tobacco yellow leaf mutations.
2024-10-23 | GSE270039 | GEO
Project description:The soil-borne bacterial pathogen Ralstonia solanacearum invades a broad range of plants through roots, resulting in wilting of the plant, but no effective protection against this disease has been developed. Two R. solanacearum resistance-inducing compounds were biochemically isolated from tobacco and identified as sclareol and cis-abienol, diterpenes. When exogenously applied to their roots, these diterpenes induced resistance to R. solanacearum in tobacco, tomato, and Arabidopsis plants without exhibiting any antimicrobial activity. Structure-activity correlation analysis of sclareol-related compounds revealed that the hydroxyl group at the eighth carbon position is responsible for the activity for inducing resistance. Microarray analysis identified many sclareol-responsive Arabidopsis genes, such as those encoding or with role in ABC transporters, biosynthesis and signaling of defense-related signal molecules, and mitogen-activated protein kinase (MAPK) cascades. Sclareol-induced R. solanacearum resistance was partially compromised in Arabidopsis mutants defective in the ABC transporter AtPDR12, the MAPK MPK3, and ethylene and abscisic acid signaling pathways. Transgenic tobacco plants in which NtPDR1, a tobacco homolog of AtPDR12, was silenced exhibited also reduced resistance. These results suggest that multiple host factors are involved in resistance to R. solanacearum induced by sclareol and its related compounds and that these compounds can be used to protect crops from bacterial wilt disease.
2011-08-19 | GSE31230 | GEO