Comprehensive RNA-seq analysis revealed gene network associated with leaf morphogenesis in Vitis vinifera

Author(s):  
Tariq Pervaiz ◽  
Muhammad Salman Haider ◽  
Haifeng Jia ◽  
Ting Zheng ◽  
Muhammad Faheem ◽  
...  
2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jie Cui ◽  
Zexi Lv ◽  
Fangzhou Teng ◽  
La Yi ◽  
Weifeng Tang ◽  
...  

Airway remodeling is one of the typical pathological characteristics of asthma, while the structural changes of the airways in asthma are complex, which impedes the development of novel asthma targeted therapy. Our previous study had shown that Bu-Shen-Yi-Qi formula (BSYQF) could ameliorate airway remodeling in chronic asthmatic mice by modulating airway inflammation and oxidative stress in the lung. In this study, we analysed the lung transcriptome of control mice and asthmatic mouse model with/without BSYQF treatment. Using RNA-sequencing (RNA-seq) analysis, we found that 264/1746 (15.1%) of transcripts showing abnormal expression in asthmatic mice were reverted back to completely or partially normal levels by BSYQF treatment. Additionally, based on previous results, we identified 21 differential expression genes (DEGs) with fold changes (FC) > (±) 2.0 related to inflammatory, oxidative stress, mitochondria, PI3K/AKT, and MAPK signal pathways which may play important roles in the mechanism of the anti-remodeling effect of BSYQF treatment. Through inputting 21 DEGs into the IPA database to construct a gene network, we inferred Adipoq, SPP1, and TNC which were located at critical nodes in the network may be key regulators of BSYQF's anti-remodeling effect. In addition, the quantitative real-time polymerase chain reaction (qRT-PCR) result for the selected four DEGs matched those of the RNA-seq analysis. Our results provide a preliminary clue to the molecular mechanism of the anti-remodeling effect of BSYQF in asthma.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 5053-5053 ◽  
Author(s):  
Manish Kohli ◽  
Liewei Wang ◽  
Scott Dehm ◽  
David W. Hillman ◽  
Hugues Sicotte ◽  
...  

5053 Background: Genomic aberrations associated with resistance/response to AA/P are not known. In a prospective study we assessed whole-exome/RNA-seq based aberrations in CRPC metastatic biopsies for identifying molecular markers associated with primary resistance and response duration. Methods: Sequencing of metastatic biopsies was performed for analyzing molecular aberrations that predict primary resistance (defined as progression at 12-weeks of therapy (non-responders) using PSA, RECIST, bone scan criteria per PCWG2). Gene network analysis was performed in genes mutated more frequently in non-responders and in genes differentially expressed between non-responders and responders using a “risk ratio” (RR) of ≥2. Cox regression models with multiple gene network pathways were used for determining association with time to treatment change (TTTC). Results: Of 92 enrolled pts 82 had complete whole-exome, RNA-seq & 12-week outcome data available for analysis. At 12-weeks 33/82 had progressed. Using a RR of ≥2, 113 genes were more frequently mutated in non-responders & 292 in responders. In non-responders, gene network analysis revealed frequent mutations in Wnt/β-catenin pathway genes; frequent deletion of negative regulators of Wnt pathway ( DKK4, SFRP2, LRP6). Gene expression analyses revealed significantly reduced expression levels of Wnt/β-catenin pathway inhibitors and increased expression levels of cell cycle proliferation (CCP) genes in non-responders. Median study follow up was 32 months during which time 58/82 pts progressed and switched treatments. Median TTTC was 10.1 months (IQR:4.4-24.1). In multivariate analysis CCP scores of ≥50 predicted shorter TTTC (HR = 2.11, 95% CI: 1.17-3.80; p = 0.01). Conclusions: In metastases Wnt/β-catenin pathway activation is associated with primary AA/P resistance and increased CCP with acquired drug resistance. These findings offer molecular based predictive biomarkers in CRPC stage treatment. Clinical trial information: NCT#01953640.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Trang T. Le ◽  
Jonathan Savitz ◽  
Hideo Suzuki ◽  
Masaya Misaki ◽  
T. Kent Teague ◽  
...  

2010 ◽  
Vol 152 (4) ◽  
pp. 1787-1795 ◽  
Author(s):  
Sara Zenoni ◽  
Alberto Ferrarini ◽  
Enrico Giacomelli ◽  
Luciano Xumerle ◽  
Marianna Fasoli ◽  
...  

2016 ◽  
Vol 6 ◽  
Author(s):  
Alexandre P. Magalhães ◽  
Nuno Verde ◽  
Francisca Reis ◽  
Inês Martins ◽  
Daniela Costa ◽  
...  

2017 ◽  
Author(s):  
Abolfazl Doostparast Torshizi ◽  
Chris Armoskus ◽  
Hanwen Zhang ◽  
Marc P. Forrest ◽  
Siwei Zhang ◽  
...  

AbstractTissue-specific reverse engineering of transcriptional networks has uncovered master regulators (MRs) of cellular networks in various cancers, yet the application of this method to neuropsychiatric disorders is largely unexplored. Here, using RNA-Seq data on postmortem dorsolateral prefrontal cortex (DLPFC) from schizophrenia (SCZ) patients and control subjects, we deconvolved the transcriptional network to identify MRs that mediate expression of a large body of target genes. Together with an independent RNA-Seq data on cultured cells derived from olfactory neuroepithelium, we identified TCF4, a leading SCZ risk locus implicated by genome-wide association studies, as one of the top candidate MRs that may be potentially dysregulated in SCZ. We validated the dysregulated TCF4-related transcriptional network through examining the transcription factor binding footprints inferred from human induced pluripotent stem cell (hiPSC)-derived neuronal ATAC-Seq data, as well as direct binding sites obtained from ChIP-seq data in SH-SY5Y cells. The predicted TCF4 transcriptional targets were enriched for genes showing transcriptomic changes upon knockdown of TCF4 in hiPSC-derived neural progenitor cells (NPC) and glutamatergic neurons (Glut_N), based on observations from three separate cell lines. The altered TCF4 gene network perturbations in NPC, as compared to that in Glut_N, was more similar to the expression differences in the TCF4 gene network observed in the DLPFC of individuals with SCZ. Moreover, TCF4-associated gene expression changes in NPC were more enriched than Glut_N for pathways involved in neuronal activity, genome-wide significant SCZ risk genes, and SCZ-associated de novo mutations. Our results suggest that TCF4 may potentially serve as a MR of a gene network that confers susceptibility to SCZ at early stage of neurodevelopment, highlighting the importance of network dysregulation involving core genes and many hundreds of peripheral genes in conferring susceptibility to neuropsychiatric diseases.


2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Hui-Yee Yong ◽  
Zhongwei Zou ◽  
Eng-Piew Kok ◽  
Bih-Hua Kwan ◽  
Kingsley Chow ◽  
...  

Amphidiploid species in the Brassicaceae family, such asBrassica napus, are more tolerant to environmental stress than their diploid ancestors. A relatively salt tolerantB. napusline, N119, identified in our previous study, was used. N119 maintained lower Na+content, and Na+/K+and Na+/Ca2+ratios in the leaves than a susceptible line. The transcriptome profiles of both the leaves and the roots 1 h and 12 h after stress were investigated.De novoassembly of individual transcriptome followed by sequence clustering yielded 161,537 nonredundant sequences. A total of 14,719 transcripts were differentially expressed in either organs at either time points. GO and KO enrichment analyses indicated that the same 49 GO terms and seven KO terms were, respectively, overrepresented in upregulated transcripts in both organs at 1 h after stress. Certain overrepresented GO term of genes upregulated at 1 h after stress in the leaves became overrepresented in genes downregulated at 12 h. A total of 582 transcription factors and 438 transporter genes were differentially regulated in both organs in response to salt shock. The transcriptome depicting gene network in the leaves and the roots regulated by salt shock provides valuable information on salt resistance genes for future application to crop improvement.


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