scholarly journals Spatio-Temporal Profiling of Metarhizium anisopliae—Responsive microRNAs Involved in Modulation of Plutella xylostella Immunity and Development

2021 ◽  
Vol 7 (11) ◽  
pp. 942
Author(s):  
Junaid Zafar ◽  
Yuxin Zhang ◽  
Junlin Huang ◽  
Shoaib Freed ◽  
Rana Fartab Shoukat ◽  
...  
Keyword(s):  
Plutella Xylostella ◽  
Metarhizium Anisopliae ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Defense Mechanism ◽  
Pathogenic Fungus ◽  
Insect Pest ◽  
Luciferase Assay ◽  
Economic Losses

Metarhizium anisopliae, a ubiquitous pathogenic fungus, regulates a wide array of the insect pest population. The fungus has been employed to control Plutella xylostella, an insecticide-resistant destructive lepidopteran pest, which causes substantial economic losses in crops worldwide. Integration of modern gene-silencing technologies in pest control strategies has become more crucial to counter pesticide-resistant insects. MicroRNAs (miRNA) play essential roles in the various biological process via post-transcriptional gene regulation. In the present study, RNA-seq analysis of control (CK36h, CK72h) and fungal-infected (T36h, T72h) midguts was performed to reveal underlying molecular mechanisms occurring in larval midgut at different time courses. We aimed at exploring M. anisopliae-responsive miRNAs and their target genes involved in development and immunity. After data filtration, a combined set of 170 miRNAs were identified from all libraries. Interestingly, miR-281, miR-263, miR-1, miR-6094 and miR-8 were listed among the most abundantly expressed conserved miRNAs. Furthermore, we experimentally studied the role of differentially expressed miR-11912-5p in regulating corresponding target trypsin-like serine proteinase (Px_TLSP). The luciferase assay (in vitro) revealed that miRNA-11912-5p significantly downregulated its target gene, suggesting it might play a crucial role in defense mechanism of P. xylostella against M.+ anisopliae infection. We used synthetic miRNA mimic/inhibitor (in vivo), to overexpress/silence miRNA, which showed harmful effects on larval duration, survival and adult fecundity. Additionally, fungal application in the presence of mimics revealed enhanced sensitivity of P. xylostella to infection. Our finding provides an insight into the relatively obscure molecular mechanisms involved in insect midgut during the fungal infection.

scholarly journals On the virulence of the entomopathogenic fungi, Beauveria bassiana and Metarhizium anisopliae (Ascomycota: Hypocreales), against the diamondback moth, Plutella xylostella (L.) (Lepidoptera: Plutellidae)

2021 ◽  
Vol 31 (1) ◽  
Author(s):  
Muhammad Shehzad ◽  
Muhammad Tariq ◽  
Tariq Mukhtar ◽  
Asim Gulzar
Keyword(s):  
Sex Ratio ◽  
Beauveria Bassiana ◽  
Entomopathogenic Fungi ◽  
Plutella Xylostella ◽  
Metarhizium Anisopliae ◽  
Insect Pest ◽  
Diamondback Moth ◽  
Economic Damage ◽  
Offspring Sex Ratio ◽  
Development Of Resistance

Abstract Background The diamondback moth, Plutella xylostella (L.) (Lepidoptera: Plutellidae), is a noxious pest of cruciferous crops all over the world causing serious economic damage. Management of insect pest generally depends on chemical control; however, due to development of resistance against all types of insecticides, alternative approaches especially utilization of a microbial agent is inevitable. Results Potential of 2 entomopathogenic fungi (EPF), viz., Beauveria bassiana and Metarhizium anisopliae, was evaluated against 2nd and 3rd larval instars of P. xylostella by adopting leaf dip and direct spraying methods under laboratory conditions. Significant mortality rate was achieved by each fungus under adopted methodologies. However, B. bassiana was found to be more effective in both conditions than M. anisopliae. Highest mean corrected mortality (77.80%) was recorded, when spores of B. bassiana were sprayed on the 2nd instar larvae (LC50=1.78×104/ml) after the 6th day of treatment. Similarly, incase of M. anisopliae LC50 for the 2nd instar at the same methodology was 2.78×104/ml with a mortality percentage of 70.0%. Offspring sex ratio was non-significantly related to treatment concentration and methodology, except for the control. Conclusion Beauveria bassiana and M. anisopliae had potential to suppress P. xylostella infestations when applied appropriately. Present findings suggested that B. bassiana and M. anisopliae when sprayed on immatures of host insect had more effect as compared to leaf dip procedure. Furthermore, no significant effect of concentrations was observed on sex ratio.

7-hydroxyfrullanolide, isolated from Sphaeranthus indicus, inhibits colorectal cancer cell growth by p53-dependent and -independent mechanism

2018 ◽  
Vol 40 (6) ◽  
pp. 791-804
Author(s):  
Praveen Pandey ◽  
Deepika Singh ◽  
Mohammad Hasanain ◽  
Raghib Ashraf ◽  
Mayank Maheshwari ◽  
...  
Keyword(s):  
Cell Growth ◽  
Anticancer Activity ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Apoptotic Pathway ◽  
Syngeneic Mouse Model ◽  
Sphaeranthus Indicus

Abstract Sphaeranthus indicus Linn. is commonly used in Indian traditional medicine for management of multiple pathological conditions. However, there are limited studies on anticancer activity of this plant and its underlying molecular mechanisms. Here, we isolated an active constituent, 7-hydroxyfrullanolide (7-HF), from the flowers of this plant, which showed promising chemotherapeutic potential. The compound was more effective in inhibiting in vitro proliferation of colon cancers cells through G2/M phase arrest than other cancer cell lines that were used in this study. Consistent with in vitro data, 7-HF caused substantial regression of tumour volume in a syngeneic mouse model of colon cancer. The molecule triggered extrinsic apoptotic pathway, which was evident as upregulation of DR4 and DR5 expression as well as induction of their downstream effector molecules (FADD, Caspase-8). Concurrent activation of intrinsic pathway was demonstrated with loss of ΔΨm to release pro-apoptotic cytochrome c from mitochondria and activation of downstream caspase cascades (Caspase -9, -3). Loss of p53 resulted in decreased sensitivity of cells towards pro-apoptotic effect of 7-HF with increased number of viable cells indicating p53-dependent arrest of cancer cell growth. This notion was further supported with 7-HF-mediated elevation of endogenous p53 level, decreased expression of MDM2 and transcriptional upregulation of p53 target genes in apoptotic pathway. However, 7-HF was equally effective in preventing progression of HCT116 p53+/+ and p53−/− cell derived xenografts in nude mice, which suggests that differences in p53 status may not influence its in vivo efficacy. Taken together, our results support 7-HF as a potential chemotherapeutic agent and provided a new mechanistic insight into its anticancer activity.

Gene Expression Analysis on the Early Development of Pig Embryos Exposed to Malathion

2007 ◽  
Vol 26 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Zayil Salazar ◽  
Yvonne Ducolomb ◽  
Miguel Betancourt ◽  
Edmundo Bonilla ◽  
Leticia Cortés ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Hypothetical Protein ◽  
Cdna Libraries ◽  
Mhc I ◽  
Vitro Fertilization ◽  
Embryo Cells ◽  
Gene Expression Alterations

Malathion is a widely used pesticide and there is evidence that it could alter mammal’s germ and somatic cells, as well as cell lines. There are not enough studies showing how the nonacute malathion doses affect gene expression. This study analyzes gene expression alterations in pig morular embryos exposed in vitro , for 96 h, to several malathion concentrations after in vitro fertilization. cDNA libraries of isolated morular embryos were created and differential screenings performed to identify target genes. Seven clones were certainly identified. Genes related to mitochondrial metabolism as cytochrome c subunits I and III, nuclear genes such as major histocompatibility complex I (MHC I), and a hypothetical protein related with a splicing factor were the target of malathion’s deregulation effect. The widespread use of malathion as a pesticide should be regarded with reproductive implications and more detailed analysis would yield more about molecular mechanisms of malathion injury on embryo cells.

scholarly journals Effects of Short-time Exposure to Atrazine on miRNA Expression Profiles in the Gonad of Common Carp (Cyprinus carpio)

2018 ◽  
Author(s):  
Fang Wang ◽  
Qian-wen Yang ◽  
Wen-Jie Zhao ◽  
Qi-Yan Du ◽  
Zhong-Jie Chang
Keyword(s):  
Common Carp ◽  
Cyprinus Carpio ◽  
Mirna Expression ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Expression Profiles ◽  
Endocrine Disrupting Chemical ◽  
Endocrine Disrupting ◽  
Mirna Expression Profiles

ABSTRACTMicroRNAs (miRNAs) are endogenous small non-coding RNAs that negatively regulate gene expression by targeting specific mRNAs; they are involved in the modulation of important mRNA networks involved in toxicity. Atrazine is a known endocrine-disrupting chemical, whose molecular mechanisms are unknown. In this study, common carp (Cyprinus carpio) gonads at two key developmental stages were exposed to 0.428 ppb atrazine for 24 h in vitro. MiRNA expression profiles were analysed to identify miRNAs related to gonad development and to reveal the atrazine mechanisms interfering with gonad differentiation. Atrazine exposure caused significant alteration of multiple miRNAs. Compared with the juvenile ovary, more miRNAs were down-regulated in juvenile testis, some of these down-regulated miRNAs target the steroid hormone biosynthesis pathway related-genes. Predicted target genes of differently-expressed miRNAs after exposure to atrazine were involved in many reproductive biology signalling pathways. We suggest that these target genes may have important roles in atrazine-induced reproductive toxicity by altering miRNAs expression. Our results also indicate that atrazine can up-regulate aromatase expression through miRNAs, which supports the hypothesis that atrazine has endocrine-disrupting activity by altering the expression of genes of the Hypothalamus-Pituitary-Gonad axis through its corresponding miRNAs. This study tells us the following conclusions: 1. Atrazine exposure results in significant alterations of miRNAs whose predicted target genes are associated with reproductive processes. 2. In the primordial gonad, atrazine promoted the expression of early gonad-determining genes by decreasing specific miRNAs. 3. In the juvenile gonad, atrazine promoted the biosynthesis of steroid hormones.

scholarly journals YTHDC1-mediated VPS25 regulates cell cycle by targeting JAK-STAT signaling in human glioma cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaolong Zhu ◽  
Hui Yang ◽  
Mengying Zhang ◽  
Xingwei Wu ◽  
Lan Jiang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Glioma Cells ◽  
Prognostic Indicator ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Endosomal Sorting ◽  
Cancer Genome Atlas

Abstract Background Glioma is a common type of malignant brain tumor with a high mortality and relapse rate. The endosomal sorting complex required for transport (ESCRT) has been reported to be involved in tumorigenesis. However, the molecular mechanisms have not been clarified. Methods Bioinformatics was used to screen the ESCRT subunits highly expressed in glioma tissues from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The function of the ESCRT subunits in glioma cells was examined in vitro. Transcriptome sequencing analyzed the target genes and signaling pathways affected by the ESCRT subunit. Finally, the relationship between m6A (N6-methyladenosine) modification and high expression of the ESCRT subunit was studied. Results VPS25 was upregulated in glioma tissues, which was correlated with poor prognosis in glioma patients. Furthermore, VPS25 knockdown inhibited the proliferation, blocked the cell cycle, and promoted apoptosis in glioma cells. Meanwhile, VPS25 induced a G0/G1 phase arrest of the cell cycle in glioma cells by directly mediating p21, CDK2, and cyclin E expression, and JAK-signal transducer and activator of transcription (STAT) activation. Finally, YTHDC1 inhibited glioma proliferation by reducing the expression of VPS25. Conclusion These results suggest that VPS25 is a promising prognostic indicator and a potential therapeutic target for glioma.

scholarly journals UJI EFIKASI BIOINSEKTISIDA JAMUR ENTOMOPATOGEN BERFORMULASI CAIR TERHADAP Plutella xylostella (L.) DI LABORATORIUM

2013 ◽  
Vol 13 (1) ◽  
pp. 52-60
Author(s):  
Haperidah Nunilahwati ◽  
Siti Herlinda ◽  
Chandra Irsan ◽  
Yulia Pujiastuti ◽  
Khodijah Khodijah ◽  
...  
Keyword(s):  
Beauveria Bassiana ◽  
Entomopathogenic Fungi ◽  
Active Ingredient ◽  
Plutella Xylostella ◽  
Metarhizium Anisopliae ◽  
Entomopathogenic Fungus ◽  
Crop Production ◽  
Insect Pest ◽  
Larval Mortality ◽  
Third Instar Larvae

Efficacy test of liquid bio-insecticide of entomopathogenic fungi in control against Plutella xylostella in the laboratory.  The insect pest P. xylostella could reduce crop production of Brassicaceae. The aim of research was to test the efficacy liquid bio insecticide with active ingredient of Beauveria bassiana and Metarhizium anisopliae fungi to control P. xylostella. Bio-insecticide was applied by spraying  on mustard leaves infested with 50 individuals of third instar larvae of P. xylostella and a density of 1x106 conidia ml-1. Larval mortality was observed every 2 hours and LT50 of larvae was calculated. The study showed that the highest percentage of mortality found in Mt ES and Mt ES (cf) isolates was 99.6%, the lowest mortality at Mt NES isolate was 96.80%. LT50 and LT95 values   Bb ES were the lowest i.e. 2.04 days and 2.95 days. The highest LT50 and LT95 of Mt NES isolate were 2.24 days and 3.32 days. The liquid bio-insecticide of entomopathogenic fungus B. bassiana and M. anisopliae were effective to control the larvae of P. xylostella.

scholarly journals Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Visnu Chaparro ◽  
Louis-Philippe Leroux ◽  
Aude Zimmermann ◽  
Armando Jardim ◽  
Brent Johnston ◽  
...  
Keyword(s):  
Visceral Leishmaniasis ◽  
Leishmania Donovani ◽  
Molecular Mechanisms ◽  
Defense Mechanism ◽  
Protozoan Parasite ◽  
Parasitic Infections ◽  
Dependent Manner ◽  
Chemokine Production ◽  
Content Type

ABSTRACT CXCL16 is a multifunctional chemokine that is highly expressed by macrophages and other immune cells in response to bacterial and viral pathogens; however, little is known regarding the role of CXCL16 during parasitic infections. The protozoan parasite Leishmania donovani is the causative agent of visceral leishmaniasis. Even though chemokine production is a host defense mechanism during infection, subversion of the host chemokine system constitutes a survival strategy adopted by the parasite. Here, we report that L. donovani promastigotes upregulate CXCL16 synthesis and secretion by bone marrow-derived macrophages (BMDM). In contrast to wild-type parasites, a strain deficient in the virulence factor lipophosphoglycan (LPG) failed to induce CXCL16 production. Consistent with this, cell treatment with purified L. donovani LPG augmented CXCL16 expression and secretion. Notably, the ability of BMDM to promote migration of cells expressing CXCR6, the cognate receptor of CXCL16, was augmented upon L. donovani infection in a CXCL16- and LPG-dependent manner. Mechanistically, CXCL16 induction by L. donovani required the activity of AKT and the mechanistic target of rapamycin (mTOR) but was independent of Toll-like receptor signaling. Collectively, these data provide evidence that CXCL16 is part of the inflammatory response elicited by L. donovani LPG in vitro. Further investigation using CXCL16 knockout mice is required to determine whether this chemokine contributes to the pathogenesis of visceral leishmaniasis and to elucidate the underlying molecular mechanisms.

scholarly journals Downregulation of MYPT1 increases tumor resistance in ovarian cancer by targeting the Hippo pathway and increasing the stemness

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Sandra Muñoz-Galván ◽  
Blanca Felipe-Abrio ◽  
Eva M. Verdugo-Sivianes ◽  
Marco Perez ◽  
Manuel P. Jiménez-García ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Hippo Pathway ◽  
Ovarian Tumors ◽  
Tumor Resistance ◽  
Functional Link ◽  
The Hippo Pathway

Abstract Background Ovarian cancer is one of the most common and malignant cancers, partly due to its late diagnosis and high recurrence. Chemotherapy resistance has been linked to poor prognosis and is believed to be linked to the cancer stem cell (CSC) pool. Therefore, elucidating the molecular mechanisms mediating therapy resistance is essential to finding new targets for therapy-resistant tumors. Methods shRNA depletion of MYPT1 in ovarian cancer cell lines, miRNA overexpression, RT-qPCR analysis, patient tumor samples, cell line- and tumorsphere-derived xenografts, in vitro and in vivo treatments, analysis of data from ovarian tumors in public transcriptomic patient databases and in-house patient cohorts. Results We show that MYPT1 (PPP1R12A), encoding myosin phosphatase target subunit 1, is downregulated in ovarian tumors, leading to reduced survival and increased tumorigenesis, as well as resistance to platinum-based therapy. Similarly, overexpression of miR-30b targeting MYPT1 results in enhanced CSC-like properties in ovarian tumor cells and is connected to the activation of the Hippo pathway. Inhibition of the Hippo pathway transcriptional co-activator YAP suppresses the resistance to platinum-based therapy induced by either low MYPT1 expression or miR-30b overexpression, both in vitro and in vivo. Conclusions Our work provides a functional link between the resistance to chemotherapy in ovarian tumors and the increase in the CSC pool that results from the activation of the Hippo pathway target genes upon MYPT1 downregulation. Combination therapy with cisplatin and YAP inhibitors suppresses MYPT1-induced resistance, demonstrating the possibility of using this treatment in patients with low MYPT1 expression, who are likely to be resistant to platinum-based therapy.

scholarly journals MiR-423-5p activated by E2F1 promotes neovascularization in diabetic retinopathy by targeting HIPK2

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Qing Xiao ◽  
Yinu Zhao ◽  
Hongjing Sun ◽  
Jia Xu ◽  
Wenjie Li ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Cell Viability ◽  
Molecular Mechanisms ◽  
Diabetic Complication ◽  
Tube Formation ◽  
Luciferase Assay ◽  
Vegf Signaling ◽  
Signaling Strategies

Abstract Background Diabetic retinopathy (DR) is a diabetic complication and the primary cause of blindness in the world. However, the treatments of DR are challenging given its complicated pathogenesis. Here, we investigated the molecular mechanisms of DR by focusing on the function of E2F1/miR-423-5p/HIPK2/HIF1α/VEGF axis. Methods Cultured retinal endothelial cells (hRMECs, hRECs) were treated with 25 mM glucose to mimic the high glucose-induced DR in vitro. Streptozotocin (STZ) was injected into mice to induce DR in mice. qRT-PCR, western blotting, immunohistochemistry, and ELISA were employed to measure levels of E2F1, miR-423-5p, HIPK2, HIF1α, and VEGF. H&E staining was utilized to examine retinal neovascularization. CCK-8 assay, transwell assay, and vascular tube formation assay were used to assess the cell viability, migration, and angiogenesis. Dual luciferase assay was performed to validate interactions between E2F1 and miR-423-5p, miR-423-5p and HIPK2. Results HG treatment increased the cell viability, migration, and angiogenesis accompanied by upregulation of E2F1, miR-423-5p, HIF1α, and VEGF levels, but reduction in HIPK2 expression. Knockdown of E2F1 or miR-423-5p suppressed the HG-induced increases in cell viability, migration, and angiogenesis. E2F1 transcriptionally activated miR-423-5p expression and miR-423-5p mimics blocked the effects of E2F1 knockdown on angiogenesis. Moreover, miR-423-5p directly targeted HIPK2 to disinhibit HIF1α/VEGF signaling. Knockdown of HIPK2 reversed the effects of miR-423-5p inhibitor on cell viability, migration, and angiogenesis. Knockdown of E2F1 suppressed neovascularization during DR in vivo. Conclusions E2F1 activates miR-423-5p transcription during DR to promote angiogenesis via suppressing HIPK2 expression to disinhibit HIF1α/VEGF signaling. Strategies targeting E2F1/miR-423-5p/HIPK2 axis could be potentially used for DR treatment.

scholarly journals The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer

2015 ◽  
Vol 36 (4) ◽  
pp. 1440-1452 ◽  
Author(s):  
Xiaoying Zhou ◽  
Feng Ye ◽  
Chengqiang Yin ◽  
Ya Zhuang ◽  
Ge Yue ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Target Genes ◽  
Human Cancer ◽  
Luciferase Assay ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
Proliferation And Invasion

Background/Aims: Non-coding RNAs including miRNA and lncRNA had been reported to regulate gene expression and were both related to cancer progression. MicroRNA-141 (miR-141) has been reported to play a role in the epithelial to mesenchymal transition (EMT) process and H19 has also been demonstrated to promote malignancy in various cancers. We aimed to determine the correlation between miR-141 and H19 and their roles in gastric cancer in this study. Methods: H19 and miR-141 expression were detected by qRT-PCR. By bioinformatic analysis and luciferase assay we examined the correlation between H19 and miR-141 in vitro. Results: H19 expression was found to be inversely correlated to miR-141 expression in gastric cancer cells and tissues. H19 promotes malignancy including proliferation and invasion whereas miR-141 suppresses malignancy in human cancer cells. MiR-141 binds to H19 in a sequence specific manner, and suppresses H19 expression and functions including proliferation and invasion. MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1. Conclusion: These results were the first to demonstrate that H19 and miR-141 could compete with each other and affect their target genes in gastric cancer, which provide important clues for understanding the key roles of lncRNA-miRNA functional network in cancer.

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