scholarly journals Transcriptome Sequencing Reveals the Traits of Spermatogenesis and Testicular Development in Large Yellow Croaker (Larimichthys crocea)

Genes ◽  
2019 ◽  
Vol 10 (12) ◽  
pp. 958
Author(s):  
Luo ◽  
Gao ◽  
Ding ◽  
Liu ◽  
Du ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Draft Genome ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Receptor Interaction ◽  
Testicular Development ◽  
Large Yellow Croaker ◽  
Larimichthys Crocea ◽  
Mitogen Activated Protein ◽  
Related Transcription Factor

Larimichthys crocea is an economically important marine fish in China. To date, the molecular mechanisms underlying testicular development and spermatogenesis in L. crocea have not been thoroughly elucidated. In this study, we conducted a comparative transcriptome analysis between testes (TES) and pooled multiple tissues (PMT) (liver, spleen, heart, and kidney) from six male individuals. More than 54 million clean reads were yielded from TES and PMT libraries. After mapping to the draft genome of L. crocea, we acquired 25,787 genes from the transcriptome dataset. Expression analyses identified a total of 3853 differentially expressed genes (DEGs), including 2194 testes-biased genes (highly expressed in the TES) and 1659 somatic-biased genes (highly expressed in the PMT). The dataset was further annotated by blasting with multi-databases. Functional genes and enrichment pathways involved in spermatogenesis and testicular development were analyzed, such as the neuroactive ligand–receptor interaction pathway, gonadotropin-releasing hormone (GnRH) and mitogen-activated protein kinase (MAPK) signaling pathways, cell cycle pathway, and dynein, kinesin, myosin, actin, heat shock protein (hsp), synaptonemal complex protein 2 (sycp2), doublesex- and mab-3-related transcription factor 1 (dmrt1), spermatogenesis-associated genes (spata), DEAD-Box Helicases (ddx), tudor domain-containing protein (tdrd), and piwi genes. The candidate genes identified by this study lay the foundation for further studies into the molecular mechanisms underlying testicular development and spermatogenesis in L. crocea.

scholarly journals TIR-1/SARM1 Inhibits Axon Regeneration

2020 ◽  
Author(s):  
Victoria Julian ◽  
Alexandra B. Byrne
Keyword(s):  
Molecular Mechanisms ◽  
Axon Regeneration ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Axon Degeneration ◽  
Signaling Cascade ◽  
Mitogen Activated Protein ◽  
Critical Insight ◽  
Insight Into ◽  
Secondary Consequence

AbstractAn injured axon has two choices, regenerate or degenerate. In many neurons, the result is catastrophic axon degeneration and a failure to regenerate. To coerce the injured nervous system to regenerate, the molecular mechanisms that regulate both axon regeneration and degeneration need to be defined. We found that TIR-1/SARM1, a key regulator of axon degeneration, inhibits regeneration of injured motor axons. Loss of tir-1 function both reduces the frequency with which severed axon fragments degenerate and increases the frequency of axon regeneration. The increased regeneration in tir-1 mutants is not a secondary consequence of its effects on degeneration. Rather, TIR-1 carries out each of these opposing functions cell autonomously by regulating independent downstream genetic pathways. While promoting axon degeneration with the DLK-1 mitogen activated protein kinase (MAPK) signaling cascade, TIR-1 inhibits axon regeneration by activating the NSY-1/ASK1 MAPK signaling cascade. Our finding that TIR-1 regulates both axon regeneration and degeneration provides critical insight into how axons coordinately regulate the two key responses to injury, consequently informing approaches to manipulate the balance between these responses towards repair.

scholarly journals Nell-1 Is a Key Functional Modulator in Osteochondrogenesis and Beyond

2019 ◽  
Vol 98 (13) ◽  
pp. 1458-1468
Author(s):  
C. Li ◽  
X. Zhang ◽  
Z. Zheng ◽  
A. Nguyen ◽  
K. Ting ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Skeletal Development ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Activated T Cells ◽  
Mitogen Activated Protein ◽  
Related Transcription Factor ◽  
Osteogenic Protein ◽  
Functional Relevance ◽  
Preclinical Animal Models

Neural EGFL-like 1 (Nell-1) is a well-studied osteogenic factor that has comparable osteogenic potency with the Food and Drug Administration–approved bone morphogenic protein 2 (BMP-2). In this review, which aims to summarize the advanced Nell-1 research in the past 10 y, we start with the correlation of structural and functional relevance of the Nell-1 protein with the identification of a specific receptor of Nell-1, contactin-associated protein-like 4 (Cntnap4), for osteogenesis. The indispensable role of Nell-1 in normal craniofacial and appendicular skeletal development and growth was also defined by using the newly developed tissue-specific Nell-1 knockout mouse lines in addition to the existing transgenic mouse models. With the achievements on Nell-1’s osteogenic therapeutic evaluations from multiple preclinical animal models for local and systemic bone regeneration, the synergistic effect of Nell-1 with BMP-2 on osteogenesis, as well as the advantages of Nell-1 as an osteogenic protein with antiadipogenic, anti-inflammatory, and provascularized characteristics over BMP-2 in bone tissue engineering, is highlighted, which lays the groundwork for the clinical trial approval of Nell-1. At the molecular level, besides the mitogen-activated protein kinase (MAPK) signaling pathway, we emphasize the significant involvement of the Wnt/β-catenin pathway as well as the key regulatory molecules Runt-related transcription factor 2 (Runx2) in Nell-1-induced osteogenesis. In addition, the involvement of Nell-1 in chondrogenesis and its relevant pathologies have been revealed with the participation of the nuclear factor of activated T cells 1 (Nfatc1), Runx3, and Indian hedgehog (Ihh) signaling pathways, although the mechanistic insights of Nell-1’s osteochondrogenic property will be continuously evolving. With this perspective, we elucidate some emerging and novel functional properties of Nell-1 in oral-dental and neural tissues that will be the frontiers of future Nell-1 studies beyond the context of bone and cartilage. As such, the therapeutic potential of Nell-1 continues to evolve and grow with continuous pursuit.

scholarly journals Uncovering the Pharmacological Mechanism of Stemazole in the Treatment of Neurodegenerative Diseases Based on a Network Pharmacology Approach

2020 ◽  
Vol 21 (2) ◽  
pp. 427 ◽  
Author(s):  
Jing Zhang ◽  
Huajun Li ◽  
Yubo Zhang ◽  
Chaoran Zhao ◽  
Yizi Zhu ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Neurodegenerative Diseases ◽  
Molecular Mechanisms ◽  
Target Prediction ◽  
Mapk Signaling ◽  
Scientific Basis ◽  
Mitogen Activated Protein Kinase ◽  
Network Pharmacology ◽  
Protective Effects ◽  
Mitogen Activated Protein

Stemazole exerts potent pharmacological effects against neurodegenerative diseases and protective effects in stem cells. However, on the basis of the current understanding, the molecular mechanisms underlying the effects of stemazole in the treatment of Alzheimer’s disease and Parkinson’s disease have not been fully elucidated. In this study, a network pharmacology-based strategy integrating target prediction, network construction, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and molecular docking was adopted to predict the targets of stemazole relevant to the treatment of neurodegenerative diseases and to further explore the involved pharmacological mechanisms. The majority of the predicted targets were highly involved in the mitogen-activated protein kinase (MAPK) signaling pathway. RAC-alpha serine/threonine-protein kinase (AKT1), caspase-3 (CASP3), caspase-8 (CASP8), mitogen-activated protein kinase 8 (MAPK8), and mitogen-activated protein kinase 14 (MAPK14) are the core targets regulated by stemazole and play a central role in its anti-apoptosis effects. This work provides a scientific basis for further elucidating the mechanism underlying the effects of stemazole in the treatment of neurodegenerative diseases.

scholarly journals Mai1 Protein Acts Between Host Recognition of Pathogen Effectors and Mitogen-Activated Protein Kinase Signaling

2019 ◽  
Vol 32 (11) ◽  
pp. 1496-1507 ◽  
Author(s):  
Robyn Roberts ◽  
Sarah R. Hind ◽  
Kerry F. Pedley ◽  
Benjamin A. Diner ◽  
Matthew J. Szarzanowicz ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Kinase Domain ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Host Recognition ◽  
Virus Induced Gene Silencing ◽  
Pathogen Effectors ◽  
Mitogen Activated Protein

The molecular mechanisms acting between host recognition of pathogen effectors by nucleotide-binding leucine-rich repeat receptor (NLR) proteins and mitogen-activated protein kinase (MAPK) signaling cascades are unknown. MAPKKKα (M3Kα) activates MAPK signaling leading to programmed cell death (PCD) associated with NLR-triggered immunity. We identified a tomato M3Kα-interacting protein, SlMai1, that has 80% amino acid identity with Arabidopsis brassinosteroid kinase 1 (AtBsk1). SlMai1 has a protein kinase domain and a C-terminal tetratricopeptide repeat domain that interacts with the kinase domain of M3Kα. Virus-induced gene silencing of Mai1 homologs in Nicotiana benthamiana increased susceptibility to Pseudomonas syringae and compromised PCD induced by four NLR proteins. PCD was restored by expression of a synthetic SlMai1 gene that resists silencing. Expression of AtBsk1 did not restore PCD in Mai1-silenced plants, suggesting SlMai1 is functionally divergent from AtBsk1. PCD caused by overexpression of M3Kα or MKK2 was unaffected by Mai1 silencing, suggesting Mai1 acts upstream of these proteins. Coexpression of Mai1 with M3Kα in leaves enhanced MAPK phosphorylation and accelerated PCD. These findings suggest Mai1 is a molecular link acting between host recognition of pathogens and MAPK signaling.

scholarly journals Ciclopirox and bortezomib synergistically inhibits glioblastoma multiforme growth via simultaneously enhancing JNK/p38 MAPK and NF-κB signaling

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Zhipeng Su ◽  
Shengnan Han ◽  
Qiumei Jin ◽  
Ningning Zhou ◽  
Junwan Lu ◽  
...  
Keyword(s):  
Glioblastoma Multiforme ◽  
Anticancer Drug ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Cellular Migration ◽  
Mitogen Activated Protein Kinase ◽  
Migration And Invasion ◽  
Mantle Cell ◽  
Mitogen Activated Protein ◽  
Tumorigenic Activity

AbstractCiclopirox (CPX) is an antifungal drug that has recently been reported to act as a potential anticancer drug. However, the effects and underlying molecular mechanisms of CPX on glioblastoma multiforme (GBM) remain unknown. Bortezomib (BTZ) is the first proteasome inhibitor-based anticancer drug approved to treat multiple myeloma and mantle cell lymphoma, as BTZ exhibits toxic effects on diverse tumor cells. Herein, we show that CPX displays strong anti-tumorigenic activity on GBM. Mechanistically, CPX inhibits GBM cellular migration and invasion by reducing N-Cadherin, MMP9 and Snail expression. Further analysis revealed that CPX suppresses the expression of several key subunits of mitochondrial enzyme complex, thus leading to the disruption of mitochondrial oxidative phosphorylation (OXPHOS) in GBM cells. In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Moreover, CPX and BTZ synergistically activates nuclear factor kappa B (NF-κB) signaling and induces cellular senescence. Our findings suggest that a combination of CPX and BTZ may serve as a novel therapeutic strategy to enhance the anticancer activity of CPX against GBM.

Molecular Networks of Seed Size Control in Plants

2019 ◽  
Vol 70 (1) ◽  
pp. 435-463 ◽  
Author(s):  
Na Li ◽  
Ran Xu ◽  
Yunhai Li
Keyword(s):  
Seed Size ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Size Control ◽  
Mapk Signaling ◽  
Research Field ◽  
Mitogen Activated Protein Kinase ◽  
Molecular Networks ◽  
Control Seed ◽  
Mitogen Activated Protein

The size of seeds affects not only evolutionary fitness but also grain yield of crops. Understanding the mechanisms controlling seed size has become an important research field in plant science. Seed size is determined by the integrated signals of maternal and zygotic tissues, which control the coordinated growth of the embryo, endosperm, and seed coat. Recent advances have identified several signaling pathways that control seed size through maternal tissues, including or involving the ubiquitin-proteasome pathway, G-protein signaling, mitogen-activated protein kinase (MAPK) signaling, phytohormone perception and homeostasis, and some transcriptional regulators. Meanwhile, growth of the zygotic tissues is regulated in part by the HAIKU (IKU) pathway and phytohormones. This review provides a general overview of current findings in seed size control and discusses the emerging molecular mechanisms and regulatory networks found to be involved.

scholarly journals Specific Functional Features of the Cell Integrity MAP Kinase Pathway in the Dimorphic Fission Yeast Schizosaccharomyces japonicus

2021 ◽  
Vol 7 (6) ◽  
pp. 482
Author(s):  
Elisa Gómez-Gil ◽  
Alejandro Franco ◽  
Beatriz Vázquez-Marín ◽  
Francisco Prieto-Ruiz ◽  
Armando Pérez-Díaz ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Environmental Changes ◽  
Yeast Species ◽  
Mapk Signaling ◽  
Fine Tuning ◽  
Mitogen Activated Protein Kinase ◽  
Major Influence ◽  
Cell Integrity ◽  
Mitogen Activated Protein ◽  
Functional Features

Mitogen activated protein kinase (MAPK) signaling pathways execute essential functions in eukaryotic organisms by transducing extracellular stimuli into adaptive cellular responses. In the fission yeast model Schizosaccharomyces pombe the cell integrity pathway (CIP) and its core effector, MAPK Pmk1, play a key role during regulation of cell integrity, cytokinesis, and ionic homeostasis. Schizosaccharomyces japonicus, another fission yeast species, shows remarkable differences with respect to S. pombe, including a robust yeast to hyphae dimorphism in response to environmental changes. We show that the CIP MAPK module architecture and its upstream regulators, PKC orthologs Pck1 and Pck2, are conserved in both fission yeast species. However, some of S. pombe’s CIP-related functions, such as cytokinetic control and response to glucose availability, are regulated differently in S. japonicus. Moreover, Pck1 and Pck2 antagonistically regulate S. japonicus hyphal differentiation through fine-tuning of Pmk1 activity. Chimeric MAPK-swapping experiments revealed that S. japonicus Pmk1 is fully functional in S. pombe, whereas S. pombe Pmk1 shows a limited ability to execute CIP functions and promote S. japonicus mycelial development. Our findings also suggest that a modified N-lobe domain secondary structure within S. japonicus Pmk1 has a major influence on the CIP signaling features of this evolutionarily diverged fission yeast.

scholarly journals Beneficial Actions of Orostachys japonica and Its Compounds against Tumors via MAPK Signaling Pathways

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 555
Author(s):  
Soyoung Hur ◽  
Eungyeong Jang ◽  
Jang-Hoon Lee
Keyword(s):  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Malignant Tumors ◽  
Treatment Options ◽  
Underlying Mechanism ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Antitumor Effects ◽  
Mesenchymal Transition ◽  
Perennial Plant

Tumors are one of the most life-threatening diseases, and a variety of cancer treatment options have been continuously introduced in order to overcome cancer and improve conventional therapy. Orostachys japonica (O. japonica), which is a perennial plant belonging to the genus Orostachys of the Crassulaceae family, has been revealed to exhibit pharmacological properties against various tumors in numerous studies. The present review aimed to discuss the biological actions and underlying molecular mechanisms of O. japonica and its representative compounds—kaempferol and quercetin—against tumors. O. japonica reportedly has antiproliferative, anti-angiogenic, and antimetastatic activities against various types of malignant tumors through the induction of apoptosis and cell cycle arrest, a blockade of downstream vascular endothelial growth factor (VEGF)-VEGFR2 pathways, and the regulation of epithelial-to-mesenchymal transition. In addition, emerging studies have highlighted the antitumor efficacy of kaempferol and quercetin. Interestingly, it was found that alterations of the mitogen-activated protein kinase (MAPK) signaling cascades are involved in the pivotal mechanisms of the antitumor effects of O. japonica and its two compounds against cancer cell overgrowth, angiogenesis, and metastasis. In summary, O. japonica could be considered a preventive and therapeutic medicinal plant which exhibits antitumor actions by reversing altered patterns of MAPK cascades, and kaempferol and quercetin might be potential components that can contribute to the efficacy and underlying mechanism of O. japonica.

scholarly journals Effect of Static Magnetic Field on Monascus ruber M7 Based on Transcriptome Analysis

2021 ◽  
Vol 7 (4) ◽  
pp. 256
Author(s):  
Shuyan Yang ◽  
Hongyi Zhou ◽  
Weihua Dai ◽  
Juan Xiong ◽  
Fusheng Chen
Keyword(s):  
Magnetic Field ◽  
Static Magnetic Field ◽  
Morphological Characteristics ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Primary Metabolism ◽  
Monascus Ruber ◽  
Growing Period ◽  
Monascus Pigments ◽  
Mitogen Activated Protein

The effects of a static magnetic field (SMF) on Monascus ruber M7 (M. ruber M7) cultured on potato dextrose agar (PDA) plates under SMF treatment at different intensities (5, 10, and 30 mT) were investigated in this paper. The results revealed that, compared with the control (CK, no SMF treatment), the SMF at all tested intensities did not significantly influence the morphological characteristics of M. ruber M7, while the intracellular and extracellular Monascus pigments (MPs) and extracellular citrinin (CIT) of M. ruber M7 were increased at 10 and 30 mT SMF but there was no impact on the MPs and CIT at 5 mT SMF. The transcriptome data of M. ruber M7 cultured at 30 mT SMF on PDA for 3 and 7 d showed that the SMF could increase the transcriptional levels of some relative genes with the primary metabolism, including the carbohydrate metabolism, amino acid metabolism, and lipid metabolism, especially in the early growing period (3 d). SMF could also affect the transcriptional levels of the related genes to the biosynthetic pathways of MPs, CIT, and ergosterol, and improve the transcription of the relative genes in the mitogen-activated protein kinase (MAPK) signaling pathway of M. ruber M7. These findings provide insights into a comprehensive understanding of the effects of SMF on filamentous fungi.

scholarly journals The Emerging Role of Macrophages in Immune System Dysfunction under Real and Simulated Microgravity Conditions

2021 ◽  
Vol 22 (5) ◽  
pp. 2333
Author(s):  
Yulong Sun ◽  
Yuanyuan Kuang ◽  
Zhuo Zuo
Keyword(s):  
Immune System ◽  
Mapk Signaling ◽  
Immune Defense ◽  
Mitogen Activated Protein Kinase ◽  
Therapeutic Drugs ◽  
Physiological Processes ◽  
Immune System Dysfunction ◽  
Cell Immunity ◽  
Mitogen Activated Protein ◽  
Microgravity Conditions

In the process of exploring space, the astronaut’s body undergoes a series of physiological changes. At the level of cellular behavior, microgravity causes significant alterations, including bone loss, muscle atrophy, and cardiovascular deconditioning. At the level of gene expression, microgravity changes the expression of cytokines in many physiological processes, such as cell immunity, proliferation, and differentiation. At the level of signaling pathways, the mitogen-activated protein kinase (MAPK) signaling pathway participates in microgravity-induced immune malfunction. However, the mechanisms of these changes have not been fully elucidated. Recent studies suggest that the malfunction of macrophages is an important breakthrough for immune disorders in microgravity. As the first line of immune defense, macrophages play an essential role in maintaining homeostasis. They activate specific immune responses and participate in large numbers of physiological activities by presenting antigen and secreting cytokines. The purpose of this review is to summarize recent advances on the dysfunction of macrophages arisen from microgravity and to discuss the mechanisms of these abnormal responses. Hopefully, our work will contribute not only to the future exploration on the immune system in space, but also to the development of preventive and therapeutic drugs against the physiological consequences of spaceflight.

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