scholarly journals Gene networks under circadian control exhibit diurnal organization in primate organs

2021 ◽  
Author(s):  
Jie Li ◽  
Pengxing Nie ◽  
Christoph Turck ◽  
Guang-Zhong Wang
Keyword(s):  
Gene Networks ◽  
Target Genes ◽  
Expression Patterns ◽  
The Body ◽  
Gene Interactions ◽  
Molecular Clocks ◽  
Circadian Control ◽  
Genes Encoding ◽  
Basic Network ◽  
Significant Disease

Mammalian organs are individually controlled by autonomous circadian clocks. At the molecular level, this process is defined by the cyclical co-expression of both core transcription factors and off-target genes across time. While interactions between these molecular clocks are likely necessary for proper homeostasis, these features remain undefined. Here, we utilize integrative analysis of a baboon diurnal transcriptome atlas to characterize the properties of gene networks under circadian control. We found that 53.4% (8,120) of baboon genes are rhythmically expressed body-wide. In addition, >30% of gene-gene interactions exhibit periodic co-expression patterns, with core circadian genes more cyclically co-expressed than others. Moreover, two basic network modes were observed at the systems level: daytime and nighttime mode. Daytime networks were enriched for genes involved in metabolism, while nighttime networks were enriched for genes associated with growth and cellular signaling. A substantial number of diseases only form significant disease modules at either daytime or nighttime. In addition, we found that 216 of 313 genes encoding products that interact with SARS-CoV-2 are rhythmically expressed throughout the body. Importantly, more than 80% of SARS-CoV-2 related genes enriched modules are rhythmically expressed, and have significant network proximities with circadian regulators. Our data suggest that synchronization amongst circadian gene networks is necessary for proper homeostatic functions and circadian regulators have close interactions with SARS-CoV-2 infection.

scholarly journals Expression patterns of GHRL, GHSR, LEP, LEPR, SST and CCK genes in the gastrointestinal tissues of Tibetan and Yorkshire pigs

2019 ◽  
Vol 64 (No. 6) ◽  
pp. 239-247
Author(s):  
Wen-Kui Sun ◽  
Chi Cheng ◽  
Rui Liu ◽  
Yi-Hui Chen ◽  
Kai Zeng ◽  
...  
Keyword(s):  
Feed Intake ◽  
Plasma Levels ◽  
Target Genes ◽  
Leptin Receptor ◽  
Expression Patterns ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Growth Difference ◽  
Yorkshire Pigs

The aim was to characterize the expression patterns of several genes in the gastrointestinal tracts of Tibetan pigs (TP) and Yorkshire pigs (YP) and to explore their correlation with digestion and growth difference of the two breeds. The body weights and growth of YP and TP were studied at 6, 12 and 24 weeks of age, and their plasma levels of ghrelin (GHRL), leptin (LEP), somatostatin (SST) and cholecystokinin (CCK) were determined by enzyme linked immunosorbent assay (ELISA). Blood and gastrointestinal sections (stomach, duodenum, jejunum, ileum, caecum and colon) were collected and assayed for mRNA expression of the six genes (GHRL, ghrelin receptor (GHSR), LEP, leptin receptor (LEPR), SST and CCK) by reverse transcription-qPCR (RT-qPCR). TP generally had higher mRNA expressions of GHSR, LEP, LEPR, SST and CCK genes compared to YP, and expressed lower levels of the GHRL gene in most tissues of the digestive tract. In both breeds, plasma levels of the expressed proteins were more closely correlated with the feed intake and growth than with mRNA levels of the target genes. Our data indicate that TP possess special gene expression patterns in the gastrointestinal tract compared to YP, which is consistent with its unique feed intake and adaptation to harsh environment.

scholarly journals Gene Expression Analysis of the Streptococcus pneumoniae Competence Regulons by Use of DNA Microarrays

2000 ◽  
Vol 182 (21) ◽  
pp. 6192-6202 ◽  
Author(s):  
Scott Peterson ◽  
Robin T. Cline ◽  
Hervé Tettelin ◽  
Vasily Sharov ◽  
Donald A. Morrison
Keyword(s):  
Streptococcus Pneumoniae ◽  
Dna Microarrays ◽  
Target Genes ◽  
Expression Patterns ◽  
In Vitro Models ◽  
Regulatory Genes ◽  
Mrna Levels ◽  
Similar Expression Pattern ◽  
Genes Encoding

ABSTRACT Competence for genetic transformation in Streptococcus pneumoniae is coordinated by the competence-stimulating peptide (CSP), which induces a sudden and transient appearance of competence during exponential growth in vitro. Models of this quorum-sensing mechanism have proposed sequential expression of several regulatory genes followed by induction of target genes encoding DNA-processing-pathway proteins. Although many genes required for transformation are known to be expressed only in response to CSP, the relative timing of their expression has not been established. Overlapping expression patterns for the genes cinA andcomD (G. Alloing, B. Martin, C. Granadel, and J. P. Claverys, Mol. Microbiol. 29:75–83, 1998) suggest that at least two distinct regulatory mechanisms may underlie the competence cycle. DNA microarrays were used to estimate mRNA levels for all known competence operons during induction of competence by CSP. The known competence regulatory operons, comAB, comCDE, andcomX, exhibited a low or zero initial (uninduced) signal, strongly increased expression during the period between 5 and 12 min after CSP addition, and a decrease nearly to original values by 15 min after initiation of exposure to CSP. The remaining competence genes displayed a similar expression pattern, but with an additional delay of approximately 5 min. In a mutant defective in ComX, which may act as an alternate sigma factor to allow expression of the target competence genes, the same regulatory genes were induced, but the other competence genes were not. Finally, examination of the expression of 60 candidate sites not previously associated with competence identified eight additional loci that could be induced by CSP.

scholarly journals Genome-wide profiling of miRNA expression patterns in tubal endometriosis

Reproduction ◽  
2019 ◽  
Vol 157 (6) ◽  
pp. 525-534 ◽  
Author(s):  
Hang Qi ◽  
Guiling Liang ◽  
Jin Yu ◽  
Xiaofeng Wang ◽  
Yan Liang ◽  
...  
Keyword(s):  
Pathway Analysis ◽  
Mirna Expression ◽  
Gene Networks ◽  
Target Genes ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Mirna Gene ◽  
Differentially Expressed ◽  
Signal Pathways ◽  
Differentially Expressed Mirnas

MicroRNA (miRNA) expression profiles in tubal endometriosis (EM) are still poorly understood. In this study, we analyzed the differential expression of miRNAs and the related gene networks and signaling pathways in tubal EM. Four tubal epithelium samples from tubal EM patients and five normal tubal epithelium samples from uterine leiomyoma patients were collected for miRNA microarray. Bioinformatics analyses, including Ingenuity Pathway Analysis (IPA), Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed. Quantitative real-time polymerase chain reaction (qRT-PCR) validation of five miRNAs was performed in six tubal epithelium samples from tubal EM and six from control. A total of 17 significantly differentially expressed miRNAs and 4343 potential miRNA-target genes involved in tubal EM were identified (fold change >1.5 and FDR-adjustedPvalue <0.05). IPA indicated connections between miRNAs, target genes and other gynecological diseases like endometrial carcinoma. GO and KEGG analysis revealed that most of the identified genes were involved in the mTOR signaling pathway, SNARE interactions in vesicular transport and endocytosis. We constructed an miRNA-gene-disease network using target gene prediction. Functional analysis showed that the mTOR pathway was connected closely to tubal EM. Our results demonstrate for the first time the differentially expressed miRNAs and the related signal pathways involved in the pathogenesis of tubal EM which contribute to elucidating the pathogenic mechanism of tubal EM-related infertility.

Comprehensive Network Analysis of the Molecular Mechanisms Associated with Sorafenib Resistance in Hepatocellular Carcinoma

2019 ◽  
Author(s):  
Xiang Cui ◽  
Chao Li ◽  
Chunshan Wei ◽  
Guangdong Tong ◽  
Yufeng Xing
Keyword(s):  
Hepatocellular Carcinoma ◽  
Transcription Factors ◽  
Differentially Expressed Genes ◽  
Gene Networks ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Differential Expression Analysis ◽  
Diagnostic Value ◽  
The Body ◽  
Differentially Expressed

Abstract Background: This research aimed to investigate the potential molecular mechanism of sorafenib resistance to hepatocellular carcinoma (HCC). Methods: Differential expression analysis were performed to identified differentially expressed genes (DEGs) in sorafenib resistant HCC. Then, a series of bioinformatic analysis were performed to explore the potential crucial molecules in sorafenib resistant HCC. For example, gene function annotation, pivot regulators prediction, ROC analysis and survival analysis. Results: There were 827 differentially expressed genes were identified. Moreover, most of the differentially expressed genes are involved in immune and inflammatory-related functions and signaling pathways. Also, 18 transcription factors were predicted to regulate the transcription factors of differentially expressed genes, which play an essential role in the regulation of dysfunctional gene networks. In target genes of transcription factors, CDK1 and CDKN1A have high diagnostic value in the resistance of hepatocellular carcinoma to sorafenib. Conclusions: TAPBP has the strongest correlation with drug resistance of hepatocellular carcinoma and the highest diagnostic efficiency. In addition, CDK1 and CDKN1A have high diagnostic value in the resistance of hepatocellular carcinoma to sorafenib. Overall, our analysis shows that a large number of gene disorders occur during the development of resistance to sorafenib in hepatocellular carcinoma, and they are associated with immune and inflammatory reactions in the body. These results provide critical theoretical references for the pathogenesis and diagnosis of sorafenib resistance.

scholarly journals Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin As a Nutritive Source of Copper

2018 ◽  
Author(s):  
Ludmila V. Puchkova ◽  
Polina S. Babich ◽  
Yulia A. Zatulovskaia ◽  
Ekaterina Y. Ilyechova ◽  
Francesca Di Sole
Keyword(s):  
Expression Patterns ◽  
Molecular Genetic ◽  
Copper Metabolism ◽  
The Body ◽  
Activity Levels ◽  
Specific Expression ◽  
Toxic Agent ◽  
Copper Transporter ◽  
Genes Encoding ◽  
Central Organ

Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a co-factor for cuproenzymes and participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body: copper absorption, distribution, and excretion. In ontogenesis, there are two types of copper metabolism: embryonic and adult, which maintain the balance of copper in each of these periods, respectively. In the liver cells, these types are characterized by specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter and proteins mediating ceruloplasmin metalation. In newborns, the molecular-genetic mechanisms responsible for copper homeostasis and the ontogenetic switch from embryonic to adult copper metabolism are highly adapted to milk ceruloplasmin as a dietary source of copper. In the mammary gland cells, the level of ceruloplasmin gene expression and the alternative splicing of its pre-mRNA govern the amount of ceruloplasmin in milk, and thus, the amount of copper absorbed by the newborn is controlled. In the newborns, absorption, distribution, and accumulation copper are adapted to milk ceruloplasmin. In the newborns, which are not breast-fed at the early stages of postnatal development, the control for alimentary copper balance is absent. We tried to focus on the neonatal consequences of a violation of the balance of copper in the mother / newborn system. Although there is still much to be learned, the time to pay attention to this problem came because the neonatal misbalance of copper may provoke the development of copper related disorders for future life.

Biological function and mode of action of nuclear xenobiotic receptors

2003 ◽  
Vol 75 (11-12) ◽  
pp. 1733-1742 ◽  
Author(s):  
J. Sonoda ◽  
R. M. Evans
Keyword(s):  
Target Genes ◽  
Constitutive Androstane Receptor ◽  
Regulatory Region ◽  
Pregnane X Receptor ◽  
Drug Clearance ◽  
The Body ◽  
Pharmaceutical Drugs ◽  
Nucleotide Polymorphisms ◽  
Cytochrome P450 Enzymes ◽  
Genes Encoding

Two related nuclear receptors, the pregnane X receptor (PXR) and the constitutive androstane receptor (CAR), act as xenobiotic sensors that protect the body from a multitude of foreign chemicals (xenobiotics) and play a central role in the metabolism and clearance of steroids and toxic endogenous lipids (endobiotics). A structurally diverse array of chemicals including pharmaceutical drugs, steroids, herbal extracts, and pesticides activate PXR or CAR. This activation results in induction of overlapping, but yet distinct drug clearance pathways consisting of cytochrome P450 enzymes, conjugating enzymes, drug transporters, and other related proteins. Similar pathways are also utilized to protect the body from toxic compounds of endogenous origin. Thus, the xenobiotic regulatory circuit contributes both to drug-drug and food-drug interactions as well as endocrine disruption. Consistent with the notion that xenobiotic receptors regulate drug clearance, single nucleotide polymorphisms (SNPs) in either the receptors themselves or receptor-binding sites in the regulatory region of genes encoding metabolic enzymes appear to contribute to the polymorphic expression of components of drug clearance pathways. Together, the xenobiotic receptors PXR and CAR confer metabolic immunity via the ability to control an integrated array of target genes.

scholarly journals Copper Metabolism of Newborns Is Adapted to Milk Ceruloplasmin as a Nutritive Source of Copper: Overview of the Current Data

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1591 ◽  
Author(s):  
Ludmila Puchkova ◽  
Polina Babich ◽  
Yulia Zatulovskaia ◽  
Ekaterina Ilyechova ◽  
Francesca Di Sole
Keyword(s):  
Expression Patterns ◽  
Molecular Genetic ◽  
Copper Metabolism ◽  
Current Data ◽  
The Body ◽  
Activity Levels ◽  
Specific Expression ◽  
Toxic Agent ◽  
Copper Transporter ◽  
Genes Encoding

Copper, which can potentially be a highly toxic agent, is an essential nutrient due to its role as a cofactor for cuproenzymes and its participation in signaling pathways. In mammals, the liver is a central organ that controls copper turnover throughout the body, including copper absorption, distribution, and excretion. In ontogenesis, there are two types of copper metabolism, embryonic and adult, which maintain the balance of copper in each of these periods of life, respectively. In the liver cells, these types of metabolism are characterized by the specific expression patterns and activity levels of the genes encoding ceruloplasmin, which is the main extracellular ferroxidase and copper transporter, and the proteins mediating ceruloplasmin metalation. In newborns, the molecular genetic mechanisms responsible for copper homeostasis and the ontogenetic switch from embryonic to adult copper metabolism are highly adapted to milk ceruloplasmin as a dietary source of copper. In the mammary gland cells, the level of ceruloplasmin gene expression and the alternative splicing of its pre-mRNA govern the amount of ceruloplasmin in the milk, and thus, the amount of copper absorbed by a newborn is controlled. In newborns, the absorption, distribution, and accumulation of copper are adapted to milk ceruloplasmin. If newborns are not breast-fed in the early stages of postnatal development, they do not have this natural control ensuring alimentary copper balance in the body. Although there is still much to be learned about the neonatal consequences of having an imbalance of copper in the mother/newborn system, the time to pay attention to this problem has arrived because the neonatal misbalance of copper may provoke the development of copper-related disorders.

scholarly journals Systematic Search for Novel Circulating Biomarkers Associated with Extracellular Vesicles in Alzheimer’s Disease: Combining Literature Screening and Database Mining Approaches

2021 ◽  
Vol 11 (10) ◽  
pp. 946
Author(s):  
David Vogrinc ◽  
Katja Goričar ◽  
Tanja Kunej ◽  
Vita Dolžan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Extracellular Vesicles ◽  
Target Gene ◽  
Target Genes ◽  
Body Fluids ◽  
The Body ◽  
Gene Interactions ◽  
Circulating Biomarkers ◽  
Risk Genes

miRNAs play an important role in neurodegenerative diseases. Many miRNA-target gene interactions (MTI) have been experimentally confirmed and associated with Alzheimer’s disease (AD). miRNAs may also be contained within extracellular vesicles (EVs), mediators of cellular communication and a potential source of circulating biomarkers in body fluids. Therefore, EV-associated miRNAs (EV-miRNAs) in peripheral blood could support earlier and less invasive AD diagnostics. We aimed to prioritize EV-related miRNA with AD-related genes and to identify the most promising candidates for novel AD biomarkers. A list of unique EV-miRNAs from the literature was combined with a known set of AD risk genes and enriched for MTI. Additionally, miRNAs associated with the AD phenotype were combined with all known target genes in MTI enrichment. Expression in different sample types was analyzed to identify AD-associated miRNAs with the greatest potential as AD circulating biomarkers. Four common MTI were observed between EV-miRNAs and AD-associated miRNAs: hsa-miR-375–APH1B, hsa-miR-107–CDC42SE2, hsa-miR-375–CELF2, and hsa-miR-107–IL6. An additional 61 out of 169 unique miRNAs (36.1%) and seven out of 84 unique MTI (8.3%), observed in the body fluids of AD patients, were proposed as very strong AD-circulating biomarker candidates. Our analysis summarized several potential novel AD biomarkers, but further studies are needed to evaluate their potential in clinical practice.

Insights into the heat-responsive transcriptional network of tomato contrasting genotypes

2021 ◽  
Vol 19 (1) ◽  
pp. 44-57
Author(s):  
Sirine Werghi ◽  
Charfeddine Gharsallah ◽  
Nishi Kant Bhardwaj ◽  
Hatem Fakhfakh ◽  
Faten Gorsane
Keyword(s):  
Heat Stress ◽  
Heat Shock ◽  
Candidate Genes ◽  
Expression Patterns ◽  
Response Strategies ◽  
Transcriptional Reprogramming ◽  
Genes Encoding ◽  
Breeding Programmes ◽  
Gene Transcripts ◽  
Resource Data

AbstractDuring recent decades, global warming has intensified, altering crop growth, development and survival. To overcome changes in their environment, plants undergo transcriptional reprogramming to activate stress response strategies/pathways. To evaluate the genetic bases of the response to heat stress, Conserved DNA-derived Polymorphism (CDDP) markers were applied across tomato genome of eight cultivars. Despite scattered genotypes, cluster analysis allowed two neighbouring panels to be discriminate. Tomato CDDP-genotypic and visual phenotypic assortment permitted the selection of two contrasting heat-tolerant and heat-sensitive cultivars. Further analysis explored differential expression in transcript levels of genes, encoding heat shock transcription factors (HSFs, HsfA1, HsfA2, HsfB1), members of the heat shock protein (HSP) family (HSP101, HSP17, HSP90) and ascorbate peroxidase (APX) enzymes (APX1, APX2). Based on discriminating CDDP-markers, a protein functional network was built allowing prediction of candidate genes and their regulating miRNA. Expression patterns analysis revealed that miR156d and miR397 were heat-responsive showing a typical inverse relation with the abundance of their target gene transcripts. Heat stress is inducing a set of candidate genes, whose expression seems to be modulated through a complex regulatory network. Integrating genetic resource data is required for identifying valuable tomato genotypes that can be considered in marker-assisted breeding programmes to improve tomato heat tolerance.

scholarly journals Two Auxinic Herbicides Affect Brassica napus Plant Hormone Levels and Induce Molecular Changes in Transcription

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1153
Author(s):  
Jutta Ludwig-Müller ◽  
Roman Rattunde ◽  
Sabine Rößler ◽  
Katja Liedel ◽  
Freia Benade ◽  
...  
Keyword(s):  
Brassica Napus ◽  
Expression Patterns ◽  
Growth Conditions ◽  
Growth Stages ◽  
Auxin Response ◽  
Time Points ◽  
Genes Encoding ◽  
Different Temperatures ◽  
Indigenous Plant ◽  
Over Time

With the introduction of the new auxinic herbicide halauxifen-methyl into the oilseed rape (Brassica napus) market, there is a need to understand how this new molecule interacts with indigenous plant hormones (e.g., IAA) in terms of crop response. The aim of this study was to investigate the molecular background by using different growth conditions under which three different auxinic herbicides were administered. These were halauxifen-methyl (Hal), alone and together with aminopyralid (AP) as well as picloram (Pic). Three different hormone classes were determined, free and conjugated indole-3-acetic acid (IAA), aminocyclopropane carboxylic acid (ACC) as a precursor for ethylene, and abscisic acid (ABA) at two different temperatures and growth stages as well as over time (2–168 h after treatment). At 15 °C growth temperature, the effect was more pronounced than at 9 °C, and generally, the younger leaves independent of the developmental stage showed a larger effect on the alterations of hormones. IAA and ACC showed reproducible alterations after auxinic herbicide treatments over time, while ABA did not. Finally, a transcriptome analysis after treatment with two auxinic herbicides, Hal and Pic, showed different expression patterns. Hal treatment leads to the upregulation of auxin and hormone responses at 48 h and 96 h. Pic treatment induced the hormone/auxin response already after 2 h, and this continued for the other time points. The more detailed analysis of the auxin response in the datasets indicate a role for GH3 genes and genes encoding auxin efflux proteins. The upregulation of the GH3 genes correlates with the increase in conjugated IAA at the same time points and treatments. Also, genes for were found that confirm the upregulation of the ethylene pathway.

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