scholarly journals Identification of Candidate Genes Associated With Hypoxia Tolerance in Trachinotus blochii Using Bulked Segregant Analysis and RNA-Seq

2021 ◽  
Vol 12 ◽  
Author(s):  
Yifan Liu ◽  
Tian Jiang ◽  
Youming Chen ◽  
Yue Gu ◽  
Feibiao Song ◽  
...  
Keyword(s):  
Amino Acid ◽  
Candidate Genes ◽  
Signaling Pathway ◽  
Hypoxia Tolerance ◽  
Receptor Signaling ◽  
Linkage Groups ◽  
Nonsynonymous Mutation ◽  
Golden Pompano ◽  
Receptor Signaling Pathway ◽  
Trachinotus Blochii

Golden Pompano (Trachinotus blochii) has rapidly developed into the one of the main valuable fish species in Chinese marine aquaculture. Due to its rapid growth, active metabolism, and high oxygen consumption, hypoxia will increase its mortality and cause serious economic losses. We constructed two experimental groups of fish with different degrees of tolerance to hypoxia, used BSR-Seq analysis based on genome and genetic linkage groups to locate SNPs and genes that were related to the differences in hypoxia tolerance. The results showed that hypoxia tolerance SNPs of golden pompano may be jointly determined by multiple linkage groups, especially linkage groups 18 and 22. There were 768 and 348 candidate genes located in the candidate regions of the brain and liver, respectively. These genes were mainly involved in anaerobic energy metabolism, stress response, immune response, waste discharge, and cell death. The prostaglandin-endoperoxide synthase 2 (PTGS2) on LG8, which is involved in the metabolism of arachidonic acid, has a G/A nonsynonymous mutation at position 20641628, and the encoded amino acid was changed from hydrophobic aspartic acid to asparaginate. The specific pathway of the RIG-I-like receptor signaling pathway in the liver may mediate the metabolic system and the immune system, linking glucose metabolism with immune regulation. The death of the hypoxia-intolerant group may be due to the accumulation of lactic acid caused by the activation of anaerobic glycolysis during the early stage of hypoxia stress, and the activation of type I interferon was inhibited, which resulted in decreased immunity. Among the genes involved in the RIG-I-like receptor signaling pathway, the CYLD Lysine 63 Deubiquitinase (CYLD) located on LG16 had a G/T nonsynonymous mutation at position 13629651, and the encoded amino acid was changed from alanine acid to valine. The interferon induced with helicase C domain 1 (Ifih1) located on LG18 has a G/C nonsynonymous mutation at position 16153700, and the encoded hydrophilic glycine was changed to hydrophobic alanine. Our findings suggest these SNPs may assist in the molecular breeding of hypoxia-tolerant golden pompano, and speculate that the balance of glucose and lipid metabolism plays a key role in Trachinotus blochii under acute hypoxia.

scholarly journals A comprehensive contribution of genes for aryl hydrocarbon receptor signaling pathway to hypertension susceptibility

2017 ◽  
Vol 27 (2) ◽  
pp. 57-69 ◽  
Author(s):  
Alexey V. Polonikov ◽  
Olga Yu. Bushueva ◽  
Irina V. Bulgakova ◽  
Maxim B. Freidin ◽  
Mikhail I. Churnosov ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Signaling Pathway ◽  
Receptor Signaling ◽  
Aryl Hydrocarbon ◽  
Receptor Signaling Pathway

Cross-talk between an activator of nuclear receptors-mediated transcription and the D1 dopamine receptor signaling pathway

2005 ◽  
Vol 80 (3) ◽  
pp. 379-385 ◽  
Author(s):  
Azriel Schmidt ◽  
Robert Vogel ◽  
Su Jane Rutledge ◽  
Evan E. Opas ◽  
Gideon A. Rodan ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Dopamine Receptor ◽  
Nuclear Receptors ◽  
Cross Talk ◽  
Receptor Signaling ◽  
D1 Dopamine Receptor ◽  
Receptor Signaling Pathway

Neuromedin U-induced anorexigenic action is mediated by the corticotropin-releasing hormone receptor-signaling pathway in goldfish

Peptides ◽  
2009 ◽  
Vol 30 (12) ◽  
pp. 2483-2486 ◽  
Author(s):  
Keisuke Maruyama ◽  
Kohei Wada ◽  
Kotaro Ishiguro ◽  
Sei-Ichi Shimakura ◽  
Tatsuya Wakasugi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hormone Receptor ◽  
Receptor Signaling ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Receptor Signaling Pathway

Zinc oxide nanoparticle disruption of store-operated calcium entry in a muscarinic receptor signaling pathway

2010 ◽  
Vol 24 (7) ◽  
pp. 1953-1961 ◽  
Author(s):  
Hsiu-Jen Wang ◽  
Anna C. Growcock ◽  
Tso-hao Tang ◽  
Jennifer O’Hara ◽  
Yue-wern Huang ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Signaling Pathway ◽  
Muscarinic Receptor ◽  
Calcium Entry ◽  
Receptor Signaling ◽  
Zinc Oxide Nanoparticle ◽  
Store Operated Calcium Entry ◽  
Receptor Signaling Pathway ◽  
Oxide Nanoparticle

scholarly journals Transcriptome Analysis for Genes Associated with Small Ruminant Lentiviruses Infection in Goats of Carpathian Breed

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2054
Author(s):  
Monika Olech ◽  
Katarzyna Ropka-Molik ◽  
Tomasz Szmatoła ◽  
Katarzyna Piórkowska ◽  
Jacek Kuźmak
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Proviral Load ◽  
Cytokine Production ◽  
Small Ruminant ◽  
Receptor Signaling ◽  
Toll Like Receptor ◽  
Receptor Signaling Pathway

Small ruminant lentiviruses (SRLV) are economically important viral pathogens of sheep and goats. SRLV infection may interfere in the innate and adaptive immunity of the host, and genes associated with resistance or susceptibility to infection with SRLV have not been fully recognized. The presence of animals with relatively high and low proviral load suggests that some host factors are involved in the control of virus replication. To better understand the role of the genes involved in the host response to SRLV infection, RNA sequencing (RNA-seq) method was used to compare whole gene expression profiles in goats carrying both a high (HPL) and low (LPL) proviral load of SRLV and uninfected animals. Data enabled the identification of 1130 significant differentially expressed genes (DEGs) between control and LPL groups: 411 between control and HPL groups and 1434 DEGs between HPL and LPL groups. DEGs detected between the control group and groups with a proviral load were found to be significantly enriched in several gene ontology (GO) terms, including an integral component of membrane, extracellular region, response to growth factor, inflammatory and innate immune response, transmembrane signaling receptor activity, myeloid differentiation primary response gene 88 (MyD88)-dependent toll-like receptor signaling pathway as well as regulation of cytokine secretion. Our results also demonstrated significant deregulation of selected pathways in response to viral infection. The presence of SRLV proviral load in blood resulted in the modification of gene expression belonging to the toll-like receptor signaling pathway, the tumor necrosis factor (TNF) signaling pathway, the cytokine-cytokine receptor interaction, the phagosome, the Ras signaling pathway, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) (PI3K-Akt) signaling pathway and rheumatoid arthritis. It is worth mentioning that the most predominant in all pathways were genes represented by toll-like receptors, tubulins, growth factors as well as interferon gamma receptors. DEGs detected between LPL and HPL groups were found to have significantly enriched regulation of signaling receptor activity, the response to toxic substances, nicotinamide adenine dinucleotide (NADH) dehydrogenase complex assembly, cytokine production, vesicle, and vacuole organization. In turn, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway tool classified DEGs that enrich molecular processes such as B and T-cell receptor signaling pathways, natural killer cell-mediated cytotoxicity, Fc gamma R-mediated phagocytosis, toll-like receptor signaling pathways, TNF, mammalian target of rapamycin (mTOR) signaling and forkhead box O (Foxo) signaling pathways, etc. Our data indicate that changes in SRLV proviral load induced altered expression of genes related to different biological processes such as immune response, inflammation, cell locomotion, and cytokine production. These findings provide significant insights into defense mechanisms against SRLV infection. Furthermore, these data can be useful to develop strategies against SRLV infection by selection of animals with reduced SRLV proviral concentration that may lead to a reduction in the spread of the virus.

scholarly journals Host Non-Coding RNA Regulates Influenza A Virus Replication

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 51
Author(s):  
Yuejiao Liao ◽  
Shouqing Guo ◽  
Geng Liu ◽  
Zhenyu Qiu ◽  
Jiamin Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Influenza A ◽  
Janus Kinase ◽  
Research Progress ◽  
Receptor Signaling ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Non Coding Rnas ◽  
Virus Interactions

Outbreaks of influenza, caused by the influenza A virus (IAV), occur almost every year in various regions worldwide, seriously endangering human health. Studies have shown that host non-coding RNA is an important regulator of host–virus interactions in the process of IAV infection. In this paper, we comprehensively analyzed the research progress on host non-coding RNAs with regard to the regulation of IAV replication. According to the regulation mode of host non-coding RNAs, the signal pathways involved, and the specific target genes, we found that a large number of host non-coding RNAs directly targeted the PB1 and PB2 proteins of IAV. Nonstructural protein 1 and other key genes regulate the replication of IAV and indirectly participate in the regulation of the retinoic acid-induced gene I-like receptor signaling pathway, toll-like receptor signaling pathway, Janus kinase signal transducer and activator of transcription signaling pathway, and other major intracellular viral response signaling pathways to regulate the replication of IAV. Based on the above findings, we mapped the regulatory network of host non-coding RNAs in the innate immune response to the influenza virus. These findings will provide a more comprehensive understanding of the function and mechanism of host non-coding RNAs in the cellular anti-virus response as well as clues to the mechanism of cell–virus interactions and the discovery of antiviral drug targets.

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