scholarly journals Herbaspirillum rubrisubalbicans as a Phytopathogenic Model to Study the Immune System of Sorghum bicolor

2020 ◽  
Vol 33 (2) ◽  
pp. 235-246
Author(s):  
Thalita Regina Tuleski ◽  
Jennifer Kimball ◽  
Fernanda P. do Amaral ◽  
Tomas P. Pereira ◽  
Michelle Zibetti Tadra-Sfeir ◽  
...  
Keyword(s):  
Sorghum Bicolor ◽  
Calcium Binding ◽  
Mitogen Activated Protein Kinase ◽  
Sequencing Analysis ◽  
Molecular Pattern ◽  
Mitogen Activated Protein ◽  
Baseline Information ◽  
Responsive Element ◽  
Plant Pathogen Interactions ◽  
Herbaspirillum Rubrisubalbicans

Herbaspirillum rubrisubalbicans is the causal agent of red stripe disease (RSD) and mottle stripe disease of sorghum and sugarcane, respectively. In all, 63 genotypes of Sorghum bicolor were inoculated with H. rubrisubalbicans, with 59 showing RSD symptoms. Quantitative trait loci (QTL) analysis in a recombinant inbred line (RIL) population identified several QTL associated with variation in resistance to RSD. RNA sequencing analysis identified a number of genes whose transcript levels were differentially regulated during H. rubrisubalbicans infection. Among those genes that responded to H. rubrisubalbicans inoculation were many involved in plant–pathogen interactions such as leucine-rich repeat receptors, mitogen-activated protein kinase 1, calcium-binding proteins, transcriptional factors (ethylene-responsive element binding factor), and callose synthase. Pretreatment of sorghum leaves with the pathogen-associated molecular pattern (PAMP) molecules flg22 and chitooctaose provided protection against subsequent challenge with the pathogen, suggesting that PAMP-triggered immunity plays an important role in the sorghum immunity response. These data present baseline information for the use of the genetically tractable H. rubrisubalbicans–sorghum pathosystem for the study of innate immunity and disease resistance in this important grain and bioenergy crop. Information gained from the use of this system is likely to be informative for other monocots, including those more intractable for experimental study (e.g., sugarcane).

scholarly journals FGIN-1-27 Inhibits Melanogenesis by Regulating Protein Kinase A/cAMP-Responsive Element-Binding, Protein Kinase C-β, and Mitogen-Activated Protein Kinase Pathways

2020 ◽  
Vol 11 ◽  
Author(s):  
Jinpeng Lv ◽  
Songzhou Jiang ◽  
Ying Yang ◽  
Ximei Zhang ◽  
Rongyin Gao ◽  
...  
Keyword(s):  
Protein Kinase ◽  
The Body ◽  
Tyrosinase Activity ◽  
Mitogen Activated Protein Kinase ◽  
Mushroom Tyrosinase ◽  
Mitogen Activated Protein ◽  
Element Binding Protein ◽  
Responsive Element

FGIN-1-27 is a synthetic mitochondrial diazepam binding inhibitor receptor (MDR) agonist that has demonstrated pro-apoptotic, anti-anxiety, and steroidogenic activity in various studies. Here we report, for the first time, the anti-melanogenic efficacy of FGIN-1-27 in vitro and in vivo. FGIN-1-27 significantly inhibited basal and α-melanocyte-stimulating hormone (α-MSH)-, 1-Oleoyl-2-acetyl-sn-glycerol (OAG)- and Endothelin-1 (ET-1)-induced melanogenesis without cellular toxicity. Mushroom tyrosinase activity assay showed that FGIN-1-27 did not directly inhibit tyrosinase activity, which suggested that FGIN-1-27 was not a direct inhibitor of tyrosinase. Although it was not capable of modulating the catalytic activity of mushroom tyrosinase in vitro, FGIN-1-27 downregulated the expression levels of key proteins that function in melanogenesis. FGIN-1-27 played these functions mainly by suppressing the PKA/CREB, PKC-β, and MAPK pathways. Once inactivated, it decreased the expression of MITF, tyrosinase, TRP-1, TRP-2, and inhibited the tyrosinase activity, finally inhibiting melanogenesis. During in vivo experiments, FGIN-1-27 inhibited the body pigmentation of zebrafish and reduced UVB-induced hyperpigmentation in guinea pig skin, but not a reduction of numbers of melanocytes. Our findings indicated that FGIN-1-27 exhibited no cytotoxicity and inhibited melanogenesis in both in vitro and in vivo models. It may prove quite useful as a safer skin-whitening agent.

scholarly journals MicroRNA-148a/b-3p regulates angiogenesis by targeting neuropilin-1 in endothelial cells

2019 ◽  
Vol 51 (11) ◽  
pp. 1-11 ◽  
Author(s):  
Hyejeong Kim ◽  
Yeongrim Ko ◽  
Hyojin Park ◽  
Haiying Zhang ◽  
Yoonjeong Jeong ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Vascular Endothelial Cell ◽  
Mitogen Activated Protein Kinase ◽  
Vegf Receptor ◽  
Sequencing Analysis ◽  
Vascular Endothelial ◽  
Filamentous Actin ◽  
Neuropilin 1 ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Abstract MicroRNAs (miRs) are crucial regulators of vascular endothelial cell (EC) functions, including migration, proliferation, and survival. However, the role of most miRs in ECs remains unknown. Using RNA sequencing analysis, we found that miR-148a/b-3p expression was significantly downregulated during the differentiation of umbilical cord blood mononuclear cells into outgrowing ECs and that decreased miR-148a/b-3p levels were closely related to EC behavior. Overexpression of miR-148a/b-3p in ECs significantly reduced migration, filamentous actin remodeling, and angiogenic sprouting. Intriguingly, the effects of decreased miR-148a/b-3p levels were augmented by treatment with vascular endothelial growth factor (VEGF). Importantly, we found that miR-148a/b-3p directly regulated neuropilin-1 (NRP1) expression by binding to its 3′-untranslated region. In addition, because NRP1 is the coreceptor for VEGF receptor 2 (VEGFR2), overexpression of miR-148a/b-3p inhibited VEGF-induced activation of VEGFR2 and inhibited its downstream pathways, as indicated by changes to phosphorylated focal adhesion kinase (FAK), extracellular signal-regulated kinase (ERK), and p38 mitogen-activated protein kinase. Collectively, our results demonstrate that miR-148a/b-3p is a direct transcriptional regulator of NRP1 that mediates antiangiogenic pathways. These data suggest that miR-148a/b-3p is a therapeutic candidate for overcoming EC dysfunction and angiogenic disorders, including ischemia, retinopathy, and tumor vascularization.

Diverse Responses Are Involved in the Defence of Arabidopsis thaliana against Turnip Crinkle Virus

2013 ◽  
Vol 68 (3-4) ◽  
pp. 148-154 ◽  
Author(s):  
Hui Yang ◽  
Shu Yuan ◽  
Yi Luo ◽  
Ji Huang ◽  
Yang-Er Chen ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Plant Hormones ◽  
Plant Defence ◽  
Mitogen Activated Protein Kinase ◽  
Turnip Crinkle Virus ◽  
Wild Type ◽  
Antagonistic Action ◽  
Pathogenesis Related ◽  
Mitogen Activated Protein ◽  
Plant Pathogen Interactions

Plant hormones play pivotal roles as signals of plant-pathogen interactions. Here, we report that exogenous application of salicylic acid (SA), jasmonic acid (JA), ethephon (ETH), and abscisic acid (ABA) can reduce Turnip crinkle virus (TCV) accumulation in systemic leaves of Arabidopsis thaliana during early infection. SA and ABA are more efficient and confer a longer-lasting resistance against TCV than JA and ETH, and the plant hormones interact in effecting the plant defence. Synergistic actions of SA and JA, and SA and ET, and an antagonistic action of SA and ABA have been observed in the Arabidopsis-TCV interaction. ABA can down-regulate the expression of the pathogenesis-related genes PR1 and PDF1.2, and compared to the wild type, it drastically reduces TCV accumulation in NahG transgenic plants and the eds5-p1 mutant, both of which do not accumulate SA. This indicates that SA signaling negatively regulates the ABA-mediated defence. ABA-induced resistance against TCV is independent of SA. We also found that mitogen-activated protein kinase 5 (MPK5) may be involved in ABA-mediated defence. These results indicate that Arabidopsis can activate distinct signals to inhibit virus accumulation. Cooperative or antagonistic crosstalk between them is pivotal for establishing disease resistance. These results show potential to enhance the plant defence against viruses by manipulating diverse hormones.

scholarly journals Overexpression of Brassica napus MPK4 Enhances Resistance to Sclerotinia sclerotiorum in Oilseed Rape

2009 ◽  
Vol 22 (3) ◽  
pp. 235-244 ◽  
Author(s):  
Zheng Wang ◽  
Han Mao ◽  
Caihua Dong ◽  
Ruiqin Ji ◽  
Li Cai ◽  
...  
Keyword(s):  
Brassica Napus ◽  
Transgenic Plants ◽  
Oilseed Rape ◽  
Sclerotinia Sclerotiorum ◽  
Mitogen Activated Protein Kinase ◽  
Economic Losses ◽  
Loss Of Function ◽  
Mitogen Activated Protein ◽  
Transgenic Oilseed Rape ◽  
Plant Pathogen Interactions

Sclerotinia sclerotiorum causes a highly destructive disease in oilseed rape (Brassica napus) resulting in significant economic losses. Studies on the Arabidopsis thaliana MPK4 loss-of-function mutant have implicated that AtMPK4 is involved in plant defense regulation, and its effect on disease resistance varies in different plant–pathogen interactions. In this study, we isolated a B. napus mitogen-activated protein kinase, BnMPK4, and found that BnMPK4 along with PDF1.2 are inducible in resistant line Zhongshuang9 but both are consistently suppressed in susceptible line 84039 after inoculation with S. sclerotiorum. Transgenic oilseed rape overexpressing BnMPK4 markedly enhances resistance to S. sclerotiorum and Botrytis cinerea. Further experiments showed that transgenic plants inhibited growth of S. sclerotiorum and constitutively activated PDF1.2 but decreased H2O2 production and constitutively suppressed PR-1 expression. Treatment of roots of the transgenic plants with H2O2 solution resulted in enhanced susceptibility to the two pathogens. Our results support the idea that MPK4 positively regulates jasmonic acid-mediated defense response, which might play an important role in resistance to S. sclerotiorum in oilseed rape.

scholarly journals Identification of Msp1-Induced Signaling Components in Rice Leaves by Integrated Proteomic and Phosphoproteomic Analysis

2019 ◽  
Vol 20 (17) ◽  
pp. 4135 ◽  
Author(s):  
Ravi Gupta ◽  
Cheol Woo Min ◽  
Yu-Jin Kim ◽  
Sun Tae Kim
Keyword(s):  
Plasma Membrane ◽  
Protein Kinase ◽  
Defense Responses ◽  
Mitogen Activated Protein Kinase ◽  
Calcium Dependent ◽  
Molecular Pattern ◽  
Mitogen Activated Protein ◽  
Dependent Protein ◽  
Rice Leaves ◽  
Respiratory Burst Oxidase

MSP1 is a Magnaporthe oryzae secreted protein that elicits defense responses in rice. However, the molecular mechanism of MSP1 action is largely elusive. Moreover, it is yet to be established whether MSP1 functions as a pathogen-associated molecular pattern (PAMP) or an effector. Here, we employed a TMT-based quantitative proteomic analysis of cytosolic as well as plasma membrane proteins to decipher the MSP1 induced signaling in rice. This approach led to the identification of 6691 proteins, of which 3049 were identified in the plasma membrane (PM), while 3642 were identified in the cytosolic fraction. A parallel phosphoproteome analysis led to the identification of 1906 phosphopeptides, while the integration of proteome and phosphoproteome data showed activation of proteins related to the proteolysis, jasmonic acid biosynthesis, redox metabolism, and MAP kinase signaling pathways in response to MSP1 treatment. Further, MSP1 induced phosphorylation of some of the key proteins including respiratory burst oxidase homologue-D (RBOHD), mitogen-activated protein kinase kinase kinase-1 (MEKK1), mitogen-activated protein kinase-3/6 (MPK3/6), calcium-dependent protein kinase (CDPK) and calmodulin (CaM) suggest activation of PAMP-triggered immunity (PTI) in response to MSP1 treatment. In essence, our results further support the functioning of MSP1 as a PAMP and provide an overview of the MSP1 induced signaling in rice leaves.

scholarly journals Modulation of Rat Cancer-Induced Bone Pain is Independent of Spinal Microglia Activity

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2740
Author(s):  
Marta Diaz-delCastillo ◽  
Rie Bager Hansen ◽  
Camilla Kristine Appel ◽  
Lykke Nielsen ◽  
Sascha Nolsøe Nielsen ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Drug Targets ◽  
Bone Pain ◽  
Intrathecal Administration ◽  
Positive Control ◽  
Mitogen Activated Protein Kinase ◽  
Disease Stage ◽  
Sprague Dawley ◽  
Morphine Administration ◽  
Mitogen Activated Protein

The dissemination of cancer to bone can cause significant cancer-induced bone pain (CIBP), severely impairing the patient’s quality of life. Several rodent models have been developed to explore the nociceptive mechanisms of CIBP, including intratibial inoculation of breast carcinoma cells in syngeneic Sprague Dawley rats. Using this model, we investigated whether resident spinal microglial cells are involved in the transmission and modulation of CIBP, a long-debated disease feature. Immunohistochemical staining of ionizing calcium-binding adaptor molecule 1 (Iba-1) and phosphorylated p38-mitogen-activated protein kinase (P-p38 MAPK) showed no spinal microglial reaction in cancer-bearing rats, independently of disease stage, sex, or carcinoma cell line. As a positive control, significant upregulation of both Iba-1 and P-p38 was observed in a rat model of neuropathic pain. Additionally, intrathecal administration of the microglial inhibitor minocycline did not ameliorate pain-like behaviors in cancer-bearing rats, in contrast to spinal morphine administration. Our results indicate that microglial reaction is not a main player in CIBP, adding to the debate that even within the same models of CIBP, significant variations are seen in disease features considered potential drug targets. We suggest that this heterogeneity may reflect the clinical landscape, underscoring the need for understanding the translational value of CIBP models.

scholarly journals Molecular Regulation of Host Defense Responses Mediated by Biological Anti-TMV Agent Ningnanmycin

Viruses ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 815 ◽  
Author(s):  
Mengnan An ◽  
Tao Zhou ◽  
Yi Guo ◽  
Xiuxiang Zhao ◽  
Yuanhua Wu
Keyword(s):  
Antiviral Activity ◽  
Calcium Binding ◽  
Defense Responses ◽  
Plant Viruses ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Systemic Resistance ◽  
Mitogen Activated Protein ◽  
Significant Enrichment ◽  
Plant Pathogen Interaction

Ningnanmycin (NNM) belongs to microbial pesticides that display comprehensive antiviral activity against plant viruses. NNM treatment has been shown to efficiently delay or suppress the disease symptoms caused by tobacco mosaic virus (TMV) infection in local-inoculated or systemic-uninoculated tobacco leaves, respectively. However, the underlying molecular mechanism of NNM-mediated antiviral activity remains to be further elucidated. In this study, 414 differentially expressed genes (DEGs), including 383 which were up-regulated and 31 down-regulated, caused by NNM treatment in TMV-infected BY-2 protoplasts, were discovered by RNA-seq. In addition, KEGG analysis indicated significant enrichment of DEGs in the plant–pathogen interaction and MAPK signaling pathway. The up-regulated expression of crucial DEGs, including defense-responsive genes, such as the receptor-like kinase FLS2, RLK1, and the mitogen-activated protein kinase kinase kinase MAPKKK, calcium signaling genes, such as the calcium-binding protein CML19, as well as phytohormone responsive genes, such as the WRKY transcription factors WRKY40 and WRKY70, were confirmed by RT-qPCR. These findings provided valuable insights into the antiviral mechanisms of NNM, which indicated that the agent induces tobacco systemic resistance against TMV via activating multiple plant defense signaling pathways.

scholarly journals Comparative transcriptome analysis reveals resistant and susceptible genes in tobacco cultivars in response to infection by Phytophthora nicotianae

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
He Meng ◽  
Mingming Sun ◽  
Zipeng Jiang ◽  
Yutong Liu ◽  
Ying Sun ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Infection Process ◽  
Phytophthora Nicotianae ◽  
Mitogen Activated Protein Kinase ◽  
Rna Seq ◽  
Transcription Activator ◽  
Calcium Dependent ◽  
Calmodulin Binding ◽  
Mitogen Activated Protein ◽  
The Rich

AbstractPhytophthora nicotianae is highly pathogenic to Solanaceous crops and is a major problem in tobacco production. The tobacco cultivar Beihart1000-1 (BH) is resistant, whereas the Xiaohuangjin 1025 (XHJ) cultivar is susceptible to infection. Here, BH and XHJ were used as models to identify resistant and susceptible genes using RNA sequencing (RNA-seq). Roots were sampled at 0, 6, 12, 24, and 60 h post infection. In total, 23,753 and 25,187 differentially expressed genes (DEGs) were identified in BH and XHJ, respectively. By mapping upregulated DEGs to the KEGG database, changes of the rich factor of “plant pathogen interaction pathway” were corresponded to the infection process. Of all the DEGs in this pathway, 38 were specifically regulated in BH. These genes included 11 disease-resistance proteins, 3 pathogenesis-related proteins, 4 RLP/RLKs, 2 CNGCs, 7 calcium-dependent protein kinases, 4 calcium-binding proteins, 1 mitogen-activated protein kinase kinase, 1 protein EDS1L, 2 WRKY transcription factors, 1 mannosyltransferase, and 1 calmodulin-like protein. By combining the analysis of reported susceptible (S) gene homologs and DEGs in XHJ, 9 S gene homologs were identified, which included 1 calmodulin-binding transcription activator, 1 cyclic nucleotide-gated ion channel, 1 protein trichome birefringence-like protein, 1 plant UBX domain-containing protein, 1 ADP-ribosylation factor GTPase-activating protein, 2 callose synthases, and 2 cellulose synthase A catalytic subunits. qRT-PCR was used to validate the RNA-seq data. The comprehensive transcriptome dataset described here, including candidate resistant and susceptible genes, will provide a valuable resource for breeding tobacco plants resistant to P. nicotianae infections.

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