scholarly journals Down-regulation of EPB41L4A-AS1 mediated the brain aging and neurodegenerative diseases via damaging synthesis of NAD+ and ATP

2021 ◽  
Author(s):  
Tingpeng Yang ◽  
Yanzhi Wang ◽  
Weijie Liao ◽  
Shikuan Zhang ◽  
Songmao Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Neurodegenerative Diseases ◽  
Differentially Expressed Genes ◽  
Brain Aging ◽  
Differential Expression Analysis ◽  
Differentially Expressed ◽  
Gene Clustering ◽  
Down Regulation ◽  
Nicotinamide Riboside ◽  
Age Related

Abstract Background: Long noncoding RNA EPB41L4A-AS1 plays a very important role in metabolism. Aging and neurodegenerative diseases are typical metabolic-related processes. As a metabolism-related lncRNA, EPB41L4A-AS may be involved in the development of brain aging and neurodegenerative diseases. In this study, we aim to reveal the mechanism of EPB41L4A-AS in aging and neurodegenerative diseases.Methods: Age-related differential expression analysis was applied on the gene expression profile of the hippocampus in the Genotype-Tissue Expression database to obtain age-related differentially expressed genes and the weighted correlation network analysis algorithm was used to construct a gene co-expression network for age-related differentially expressed genes to obtain different gene clustering modules. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, protein-protein interaction network, and correlation analysis were used to reveal the mechanism of EPB41L4A-AS1. The mechanism was verified using Gene Expression Omnibus profile GSE5281 and biology experiments (construction of cell lines, Real-time quantitative PCR, Western blot, measurement of ATP and NAD+ levels, nicotinamide riboside treatment, Chromatin Immunoprecipitation) in neurons and glial-derived cells.Results: EPB41L4A-AS1 is down-regulated in aging and Alzheimer’s disease. EPB41L4A-AS1 related genes are genes of the electron transport chain and NAD+ synthesis pathway. Furthermore, these genes are highly related to neurodegenerative diseases and EPB41L4A-AS1 has a positive correlation with them. In addition, biology experiments proved that the down-regulation of EPB41L4A-AS1 can reduce the expression of these genes via modification of the acetylation of lysine 27 on histone 3, resulting in the down-regulation of NAD+ and ATP levels, while the overexpression of EPB41L4A-AS1 and nicotinamide riboside treatment can restore the levels of NAD+ and ATP.Conclusions: Down-regulation of EPB41L4A-AS1 not only disturbs NAD+ biosynthesis but also affects ATP production. As a result, the high demand of brain for NAD+ and ATP can not be met, which promotes the development of brain aging and neurodegenerative diseases. However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 down-regulation mediated decrease of NAD+ and ATP synthesis. Our results provide a new perspective on brain aging and neurodegenerative diseases.

scholarly journals Down-regulation of EPB41L4A-AS1 mediated the brain aging and neurodegenerative diseases via damaging synthesis of NAD+ and ATP

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tingpeng Yang ◽  
Yanzhi Wang ◽  
Weijie Liao ◽  
Shikuan Zhang ◽  
Songmao Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Neurodegenerative Diseases ◽  
Differentially Expressed Genes ◽  
Brain Aging ◽  
Atp Synthesis ◽  
Differentially Expressed ◽  
Gene Clustering ◽  
Nicotinamide Riboside ◽  
Atp Levels ◽  
The Brain

Abstract Background Aging and neurodegenerative diseases are typical metabolic-related processes. As a metabolism-related long non-coding RNA, EPB41L4A-AS has been reported to be potentially involved in the development of brain aging and neurodegenerative diseases. In this study, we sought to reveal the mechanisms of EPB41L4A-AS in aging and neurodegenerative diseases. Methods Human hippocampal gene expression profiles downloaded from the Genotype-Tissue Expression database were analyzed to obtain age-stratified differentially expressed genes; a weighted correlation network analysis algorithm was then used to construct a gene co-expression network of these differentially expressed genes to obtain gene clustering modules. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, protein–protein interaction network, and correlation analysis were used to reveal the role of EPB41L4A-AS1. The mechanism was verified using Gene Expression Omnibus dataset GSE5281 and biological experiments (construction of cell lines, Real-time quantitative PCR, Western blot, measurement of ATP and NAD+ levels, nicotinamide riboside treatment, Chromatin Immunoprecipitation) in neurons and glial-derived cells. Results EPB41L4A-AS1 was downregulated in aging and Alzheimer's disease. EPB41L4A-AS1 related genes were found to be enriched in the electron transport chain and NAD+ synthesis pathway. Furthermore, these genes were highly associated with neurodegenerative diseases and positively correlated with EPB41L4A-AS1. In addition, biological experiments proved that the downregulation of EPB41L4A-AS1 could reduce the expression of these genes via histone H3 lysine 27 acetylation, resulting in decreased NAD+ and ATP levels, while EPB41L4A-AS1 overexpression and nicotinamide riboside treatment could restore the NAD+ and ATP levels. Conclusions Downregulation of EPB41L4A-AS1 not only disturbs NAD+ biosynthesis but also affects ATP synthesis. As a result, the high demand for NAD+ and ATP in the brain cannot be met, promoting the development of brain aging and neurodegenerative diseases. However, overexpression of EPB41L4A-AS1 and nicotinamide riboside, a substrate of NAD+ synthesis, can reduce EPB41L4A-AS1 downregulation-mediated decrease of NAD+ and ATP synthesis. Our results provide new perspectives on the mechanisms underlying brain aging and neurodegenerative diseases.

scholarly journals A Computational Framework to Identify Transcriptional and Network Differences between Hepatocellular Carcinoma and Normal Liver Tissue and Their Applications in Repositioning Drugs

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Aimin Hu ◽  
Zheng Wei ◽  
Zuxiang Zheng ◽  
Bichao Luo ◽  
Jieming Yi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Differentially Expressed Genes ◽  
Expression Analysis ◽  
Molecular Mechanisms ◽  
Drug Repositioning ◽  
Differential Expression Analysis ◽  
Differentially Expressed ◽  
Computational Framework ◽  
Normal Tissues

Hepatocellular carcinoma (HCC) is one of the most common and lethal malignancies worldwide. Although there have been extensive studies on the molecular mechanisms of its carcinogenesis, FDA-approved drugs for HCC are rare. Side effects, development time, and cost of these drugs are the major bottlenecks, which can be partially overcome by drug repositioning. In this study, we developed a computational framework to study the mechanisms of HCC carcinogenesis, in which drug perturbation-induced gene expression signatures were utilized for repositioning of potential drugs. Specifically, we first performed differential expression analysis and coexpression network module analysis on the HCC dataset from The Cancer Genome Atlas database. Differential gene expression analysis identified 1,337 differentially expressed genes between HCC and adjacent normal tissues, which were significantly enriched in functions related to various pathways, including α-adrenergic receptor activity pathway and epinephrine binding pathway. Weighted gene correlation network analysis (WGCNA) suggested that the number of coexpression modules was higher in HCC tissues than in normal tissues. Finally, by correlating differentially expressed genes with drug perturbation-related signatures, we prioritized a few potential drugs, including nutlin and eribulin, for the treatment of hepatocellular carcinoma. The drugs have been reported by a few experimental studies to be effective in killing cancer cells.

scholarly journals UNIQUE GENE EXPRESSION IN GUT-DERIVED PHAGOCYTIC IMMUNE CELLS FROM IBD PATIENTS

2021 ◽  
Vol 27 (Supplement_1) ◽  
pp. S31-S32
Author(s):  
Gillian Jacobsen ◽  
Irina Fernandez ◽  
Maria Alejandra Quintero Cusguen ◽  
Ana Santander ◽  
Judith Pignac-Kobinger ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differentially Expressed Genes ◽  
Immune Cells ◽  
Differential Expression Analysis ◽  
Cell Activity ◽  
Acid Synthesis ◽  
Differentially Expressed ◽  
Patient Treatment ◽  
Phagocytic Cells ◽  
Immune Pathways

Abstract Introduction/Aim Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), have a complex immunopathogenesis involving chronic, dysregulated inflammation of the gut in response to commensal microbes. Current therapies, such as Anti-TNF drugs, target this immune dysregulation, but many patients exhibit recurrent inflammation despite treatment (refractoriness). Research shows that IBD patient phagocytic immune cells have altered cytokine production and bacterial clearing defects. We thus set out to analyze the transcriptome of phagocytic cells (CD11b+) isolated from patient gut biopsies. To shed light on potential causes of refractoriness, we examined cells from both not inflamed (successfully treated) and inflamed (refractory) patients on Anti-TNF therapy. Methods We used magnetic sorting to isolate CD11b+ cells from the lamina propria of a diverse set of IBD patient biopsies and performed RNA sequencing (n = 61). We used differential expression analysis to compare combinations of four patient biopsy variables: location (ileum or colon), condition (inflamed or uninflamed), IBD type (CD or UC), and patient treatment (Anti-TNF therapy or other). We also performed pathway analysis on genes significantly upregulated or downregulated (p < 0.05) between these variables. Results The highest number of differentially expressed genes was found in the colon (5578 genes upregulated) vs ileum (5582). Genes upregulated in colon mapped to innate immune pathways, while ileum pathways were mainly metabolic. Only 29 genes were differentially expressed in UC vs CD, regardless of inflammation status or location. 26 genes were differentially expressed between inflamed and uninflamed biopsies on Anti-TNF therapy (n = 16). Genes upregulated in inflamed biopsies were associated with neutrophils, while genes in uninflamed biopsies were associated with adaptive immunity, short chain fatty acid synthesis, transcription and translation, and protein secretion. Conclusion CD11b+ cells of the colon are more immunologically active, likely due to their interaction with the dense microbiome of the colon. In contrast, the metabolic pathways upregulated in ileum may point to a role for phagocytes in digestion and metabolism. These results suggest that intestinal CD11b+ gene expression is highly influenced by regional microenvironment. Fewer differences were seen comparing CD11b+ cells from CD vs UC, suggesting that this cell population is not solely responsible for the clinical differences between these diseases. The small number of differentially expressed genes in Anti-TNF refractoriness shows a clear difference between innate and adaptive immune pathways, as well as increased general cell activity in Anti-TNF responders. These genes should be further investigated to determine their precise role in refractoriness.

scholarly journals Differential gene expression analysis of ankylosing spondylitis shows deregulation of the HLA-DRB, HLA-DQB, ITM2A, and CTLA4 genes

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Rowan AlEjielat ◽  
Anas Khaleel ◽  
Amneh H. Tarkhan
Keyword(s):  
Gene Expression ◽  
Ankylosing Spondylitis ◽  
Differentially Expressed Genes ◽  
Gene Network ◽  
Disease Diagnosis ◽  
Receptor Activation ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Inflammatory Disorder ◽  
Data Set

Abstract Background Ankylosing spondylitis (AS) is a rare inflammatory disorder affecting the spinal joints. Although we know some of the genetic factors that are associated with the disease, the molecular basis of this illness has not yet been fully elucidated, and the genes involved in AS pathogenesis have not been entirely identified. The current study aimed at constructing a gene network that may serve as an AS gene signature and biomarker, both of which will help in disease diagnosis and the identification of therapeutic targets. Previously published gene expression profiles of 16 AS patients and 16 gender- and age-matched controls that were profiled on the Illumina HumanHT-12 V3.0 Expression BeadChip platform were mined. Patients were Portuguese, 21 to 64 years old, were diagnosed based on the modified New York criteria, and had Bath Ankylosing Spondylitis Disease Activity Index scores > 4 and Bath Ankylosing Spondylitis Functional Index scores > 4. All patients were receiving only NSAIDs and/or sulphasalazine. Functional enrichment and pathway analysis were performed to create an interaction network of differentially expressed genes. Results ITM2A, ICOS, VSIG10L, CD59, TRAC, and CTLA-4 were among the significantly differentially expressed genes in AS, but the most significantly downregulated genes were the HLA-DRB6, HLA-DRB5, HLA-DRB4, HLA-DRB3, HLA-DRB1, HLA-DQB1, ITM2A, and CTLA-4 genes. The genes in this study were mostly associated with the regulation of the immune system processes, parts of cell membrane, and signaling related to T cell receptor and antigen receptor, in addition to some overlaps related to the IL2 STAT signaling, as well as the androgen response. The most significantly over-represented pathways in the data set were associated with the “RUNX1 and FOXP3 which control the development of regulatory T lymphocytes (Tregs)” and the “GABA receptor activation” pathways. Conclusions Comprehensive gene analysis of differentially expressed genes in AS reveals a significant gene network that is involved in a multitude of important immune and inflammatory pathways. These pathways and networks might serve as biomarkers for AS and can potentially help in diagnosing the disease and identifying future targets for treatment.

scholarly journals Behavioral sensitization induced by methamphetamine causes differential alterations in gene expression and histone acetylation of the prefrontal cortex in rats

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hui Li ◽  
Jing-An Chen ◽  
Qian-Zhi Ding ◽  
Guan-Yi Lu ◽  
Ning Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prefrontal Cortex ◽  
Histone Acetylation ◽  
Differentially Expressed Genes ◽  
Behavioral Sensitization ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Adult Rats ◽  
Mrna Microarray ◽  
H3 Acetylation

Abstract Background Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats. Methods We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays. Results In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 genes were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure. Conclusions The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.

scholarly journals Impact of aging on gene expression response to x-ray irradiation using mouse blood

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Constantinos G. Broustas ◽  
Axel J. Duval ◽  
Sally A. Amundson
Keyword(s):  
Gene Expression ◽  
Differentially Expressed Genes ◽  
Differentially Expressed ◽  
X Rays ◽  
Gene Expression Response ◽  
X Ray ◽  
The Impact ◽  
Old Mice ◽  
Radiation Biodosimetry ◽  
Young Mice

AbstractAs a radiation biodosimetry tool, gene expression profiling is being developed using mouse and human peripheral blood models. The impact of dose, dose-rate, and radiation quality has been studied with the goal of predicting radiological tissue injury. In this study, we determined the impact of aging on the gene expression profile of blood from mice exposed to radiation. Young (2 mo) and old (21 mo) male mice were irradiated with 4 Gy x-rays, total RNA was isolated from whole blood 24 h later, and subjected to whole genome microarray analysis. Pathway analysis of differentially expressed genes revealed young mice responded to x-ray exposure by significantly upregulating pathways involved in apoptosis and phagocytosis, a process that eliminates apoptotic cells and preserves tissue homeostasis. In contrast, the functional annotation of senescence was overrepresented among differentially expressed genes from irradiated old mice without enrichment of phagocytosis pathways. Pathways associated with hematologic malignancies were enriched in irradiated old mice compared with irradiated young mice. The fibroblast growth factor signaling pathway was underrepresented in older mice under basal conditions. Similarly, brain-related functions were underrepresented in unirradiated old mice. Thus, age-dependent gene expression differences should be considered when developing gene signatures for use in radiation biodosimetry.

scholarly journals Construction of a competitive endogenous RNA network and analysis of potential regulatory axis targets in glioblastoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kai Yu ◽  
Huan Yang ◽  
Qiao-li Lv ◽  
Li-chong Wang ◽  
Zi-long Tan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Differentially Expressed Genes ◽  
Pearson Correlation ◽  
Differentially Expressed ◽  
Migration And Invasion ◽  
Glioblastoma Cells ◽  
Network Chain ◽  
Cerna Network ◽  
Potential Marker

Abstract Background Glioblastoma is the most common primary malignant brain tumor. Because of the limited understanding of its pathogenesis, the prognosis of glioblastoma remains poor. This study was conducted to explore potential competing endogenous RNA (ceRNA) network chains and biomarkers in glioblastoma by performing integrated bioinformatics analysis. Methods Transcriptome expression data from The Cancer Genome Atlas database and Gene Expression Omnibus were analyzed to identify differentially expressed genes between glioblastoma and normal tissues. Biological pathways potentially associated with the differentially expressed genes were explored by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, and a protein-protein interaction network was established using the STRING database and Cytoscape. Survival analysis using Gene Expression Profiling Interactive Analysis was based on the Kaplan–Meier curve method. A ceRNA network chain was established using the intersection method to align data from four databases (miRTarBase, miRcode, TargetScan, and lncBace2.0), and expression differences and correlations were verified by quantitative reverse-transcription polymerase chain reaction analysis and by determining the Pearson correlation coefficient. Additionally, an MTS assay and the wound-healing and transwell assays were performed to evaluate the effects of complement C1s (C1S) on the viability and migration and invasion abilities of glioblastoma cells, respectively. Results We detected 2842 differentially expressed (DE) mRNAs, 2577 DE long non-coding RNAs (lncRNAs), and 309 DE microRNAs (miRNAs) that were dysregulated in glioblastoma. The final ceRNA network consisted of six specific lncRNAs, four miRNAs, and four mRNAs. Among them, four DE mRNAs and one DE lncRNA were correlated with overall survival (p < 0.05). C1S was significantly correlated with overall survival (p= 0.015). In functional assays, knockdown of C1S inhibited the proliferation and invasion of glioblastoma cell lines. Conclusions We established four ceRNA networks that may influence the occurrence and development of glioblastoma. Among them, the MIR155HG/has-miR-129-5p/C1S axis is a potential marker and therapeutic target for glioblastoma. Knockdown of C1S inhibited the proliferation, migration, and invasion of glioblastoma cells. These findings clarify the role of the ceRNA regulatory network in glioblastoma and provide a foundation for further research.

scholarly journals AB0005 IDENTIFICATION OF KEY GENES AND PATHWAYS FOR PSORIASIS BASED ON GEO DATABASES BY BIOINFORMATICS ANALYSIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1037.2-1038
Author(s):  
X. Sun ◽  
S. X. Zhang ◽  
S. Song ◽  
T. Kong ◽  
C. Zheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Differentially Expressed Genes ◽  
Enrichment Analysis ◽  
Differentially Expressed ◽  
Shanxi Province ◽  
Receptor Interaction ◽  
Term Therapy ◽  
Pathway Enrichment Analysis ◽  
Key Genes

Background:Psoriasis is an immune-mediated, genetic disease manifesting in the skin or joints or both, and also has a strong genetic predisposition and autoimmune pathogenic traits1. The hallmark of psoriasis is sustained inflammation that leads to uncontrolled keratinocyte proliferation and dysfunctional differentiation. And it’s also a chronic relapsing disease, which often necessitates a long-term therapy2.Objectives:To investigate the molecular mechanisms of psoriasis and find the potential gene targets for diagnosis and treating psoriasis.Methods:Total 334 gene expression data of patients with psoriasis research (GSE13355 GSE14905 and GSE30999) were obtained from the Gene Expression Omnibus database. After data preprocessing and screening of differentially expressed genes (DEGs) by R software. Online toll Metascape3 was used to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs. Interactions of proteins encoded by DEGs were discovered by Protein-protein interaction network (PPI) using STRING online software. Cytoscape software was utilized to visualize PPI and the degree of each DEGs was obtained by analyzing the topological structure of the PPI network.Results:A total of 611 DEGs were found to be differentially expressed in psoriasis. GO analysis revealed that up-regulated DEGs were mostly associated with defense and response to external stimulus while down-regulated DEGs were mostly associated with metabolism and synthesis of lipids. KEGG enrichment analysis suggested they were mainly enriched in IL-17 signaling, Toll-like receptor signaling and PPAR signaling pathways, Cytokine-cytokine receptor interaction and lipid metabolism. In addition, top 9 key genes (CXCL10, OASL, IFIT1, IFIT3, RSAD2, MX1, OAS1, IFI44 and OAS2) were identified through Cytoscape.Conclusion:DEGs of psoriasis may play an essential role in disease development and may be potential pathogeneses of psoriasis.References:[1]Boehncke WH, Schon MP. Psoriasis. Lancet 2015;386(9997):983-94. doi: 10.1016/S0140-6736(14)61909-7 [published Online First: 2015/05/31].[2]Zhang YJ, Sun YZ, Gao XH, et al. Integrated bioinformatic analysis of differentially expressed genes and signaling pathways in plaque psoriasis. Mol Med Rep 2019;20(1):225-35. doi: 10.3892/mmr.2019.10241 [published Online First: 2019/05/23].[3]Zhou Y, Zhou B, Pache L, et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets. Nat Commun 2019;10(1):1523. doi: 10.1038/s41467-019-09234-6 [published Online First: 2019/04/05].Acknowledgements:This project was supported by National Science Foundation of China (82001740), Open Fund from the Key Laboratory of Cellular Physiology (Shanxi Medical University) (KLCP2019) and Innovation Plan for Postgraduate Education in Shanxi Province (2020BY078).Disclosure of Interests:None declared

scholarly journals Transcriptome Analysis of Differentially Expressed mRNA Related to Pigeon Muscle Development

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2311
Author(s):  
Hao Ding ◽  
Yueyue Lin ◽  
Tao Zhang ◽  
Lan Chen ◽  
Genxi Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Differentially Expressed Genes ◽  
Growth And Development ◽  
Muscle Development ◽  
Expression Patterns ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Growth Stages ◽  
Gene Expression And Regulation

The mechanisms behind the gene expression and regulation that modulate the development and growth of pigeon skeletal muscle remain largely unknown. In this study, we performed gene expression analysis on skeletal muscle samples at different developmental and growth stages using RNA sequencing (RNA−Seq). The differentially expressed genes (DEGs) were identified using edgeR software. Weighted gene co−expression network analysis (WGCNA) was used to identify the gene modules related to the growth and development of pigeon skeletal muscle based on DEGs. A total of 11,311 DEGs were identified. WGCNA aggregated 11,311 DEGs into 12 modules. Black and brown modules were significantly correlated with the 1st and 10th day of skeletal muscle growth, while turquoise and cyan modules were significantly correlated with the 8th and 13th days of skeletal muscle embryonic development. Four mRNA−mRNA regulatory networks corresponding to the four significant modules were constructed and visualised using Cytoscape software. Twenty candidate mRNAs were identified based on their connectivity degrees in the networks, including Abca8b, TCONS−00004461, VWF, OGDH, TGIF1, DKK3, Gfpt1 and RFC5, etc. A KEGG pathway enrichment analysis showed that many pathways were related to the growth and development of pigeon skeletal muscle, including PI3K/AKT/mTOR, AMPK, FAK, and thyroid hormone pathways. Five differentially expressed genes (LAST2, MYPN, DKK3, B4GALT6 and OGDH) in the network were selected, and their expression patterns were quantified by qRT−PCR. The results were consistent with our sequencing results. These findings could enhance our understanding of the gene expression and regulation in the development and growth of pigeon muscle.

scholarly journals Analysis of Transcriptional Changes in Different Brassica napus Synthetic Allopolyploids

Genes ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 82
Author(s):  
Yunxiao Wei ◽  
Guoliang Li ◽  
Shujiang Zhang ◽  
Shifan Zhang ◽  
Hui Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brassica Napus ◽  
Differentially Expressed Genes ◽  
Expression Patterns ◽  
Female Parent ◽  
Enrichment Analysis ◽  
Differentially Expressed ◽  
Transcriptional Changes ◽  
Aa Genome ◽  
High Degree

Allopolyploidy is an evolutionary and mechanistically intriguing process involving the reconciliation of two or more sets of diverged genomes and regulatory interactions, resulting in new phenotypes. In this study, we explored the gene expression patterns of eight F2 synthetic Brassica napus using RNA sequencing. We found that B. napus allopolyploid formation was accompanied by extensive changes in gene expression. A comparison between F2 and the parent shows a certain proportion of differentially expressed genes (DEG) and activation\silent gene, and the two genomes (female parent (AA)\male parent (CC) genomes) showed significant differences in response to whole-genome duplication (WGD); non-additively expressed genes represented a small portion, while Gene Ontology (GO) enrichment analysis showed that it played an important role in responding to WGD. Besides, genome-wide expression level dominance (ELD) was biased toward the AA genome, and the parental expression pattern of most genes showed a high degree of conservation. Moreover, gene expression showed differences among eight individuals and was consistent with the results of a cluster analysis of traits. Furthermore, the differential expression of waxy synthetic pathways and flowering pathway genes could explain the performance of traits. Collectively, gene expression of the newly formed allopolyploid changed dramatically, and this was different among the selfing offspring, which could be a prominent cause of the trait separation. Our data provide novel insights into the relationship between the expression of differentially expressed genes and trait segregation and provide clues into the evolution of allopolyploids.

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