scholarly journals Transcriptome Profiling of Starvation in the Peripheral Chemosensory Organs of the Crop Pest Spodoptera littoralis Caterpillars

Insects ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 573
Author(s):  
Erwan Poivet ◽  
Aurore Gallot ◽  
Nicolas Montagné ◽  
Pavel Senin ◽  
Christelle Monsempès ◽  
...  
Keyword(s):  
Spodoptera Littoralis ◽  
Transcriptional Response ◽  
Transcriptome Profiling ◽  
Olfactory Receptor Neuron ◽  
Immune Defense ◽  
Neuron Response ◽  
Transcriptional Changes ◽  
Food Conditions ◽  
Underlying Mechanisms ◽  
Chemosensory Organs

Starvation is frequently encountered by animals under fluctuating food conditions in nature, and response to it is vital for life span. Many studies have investigated the behavioral and physiological responses to starvation. In particular, starvation is known to induce changes in olfactory behaviors and olfactory sensitivity to food odorants, but the underlying mechanisms are not well understood. Here, we investigated the transcriptional changes induced by starvation in the chemosensory tissues of the caterpillar Spodoptera littoralis, using Illumina RNA sequencing. Gene expression profiling revealed 81 regulated transcripts associated with several biological processes, such as glucose metabolism, immune defense, response to stress, foraging activity, and olfaction. Focusing on the olfactory process, we observed changes in transcripts encoding proteins putatively involved in the peri-receptor events, namely, chemosensory proteins and odorant-degrading enzymes. Such modulation of their expression may drive fluctuations in the dynamics and the sensitivity of the olfactory receptor neuron response. In combination with the enhanced presynaptic activity mediated via the short neuropeptide F expressed during fasting periods, this could explain an enhanced olfactory detection process. Our observations suggest that a coordinated transcriptional response of peripheral chemosensory organs participates in the regulation of olfactory signal reception and olfactory-driven behaviors upon starvation.

scholarly journals Heparan Sulfate Deficiency in Cartilage: Enhanced BMP-Sensitivity, Proteoglycan Production and an Anti-Apoptotic Expression Signature after Loading

2021 ◽  
Vol 22 (7) ◽  
pp. 3726
Author(s):  
Matthias Gerstner ◽  
Ann-Christine Severmann ◽  
Safak Chasan ◽  
Andrea Vortkamp ◽  
Wiltrud Richter
Keyword(s):  
Heparan Sulfate ◽  
Pain Perception ◽  
Biological Process ◽  
Transcriptome Profiling ◽  
Mrna Levels ◽  
Unconfined Compression ◽  
Expression Signature ◽  
Hypomorphic Allele ◽  
Underlying Mechanisms ◽  
Engineered Cartilage

Osteoarthritis (OA) represents one major cause of disability worldwide still evading efficient pharmacological or cellular therapies. Severe degeneration of extracellular cartilage matrix precedes the loss of mobility and disabling pain perception in affected joints. Recent studies showed that a reduced heparan sulfate (HS) content protects cartilage from degradation in OA-animal models of joint destabilization but the underlying mechanisms remained unclear. We aimed to clarify whether low HS-content alters the mechano-response of chondrocytes and to uncover pathways relevant for HS-related chondro-protection in response to loading. Tissue-engineered cartilage with HS-deficiency was generated from rib chondrocytes of mice carrying a hypomorphic allele of Exostosin 1 (Ext1), one of the main HS-synthesizing enzymes, and wildtype (WT) littermate controls. Engineered cartilage matured for 2 weeks was exposed to cyclic unconfined compression in a bioreactor. The molecular loading response was determined by transcriptome profiling, bioinformatic data processing, and qPCR. HS-deficient chondrocytes expressed 3–6% of WT Ext1-mRNA levels. Both groups similarly raised Sox9, Col2a1, and Acan levels during maturation. However, HS-deficient chondrocytes synthesized and deposited 50% more GAG/DNA. TGFβ and FGF2-sensitivity of Ext1gt/gt chondrocytes was similar to WT cells but their response to BMP-stimulation was enhanced. Loading induced similar activation of mechano-sensitive ERK and P38-signaling in WT and HS-reduced chondrocytes. Transcriptome analysis reflected regulation of cell migration as major load-induced biological process with similar stimulation of common (Fosl1, Itgα5, Timp1, and Ngf) as well as novel mechano-regulated genes (Inhba and Dhrs9). Remarkably, only Ext1-hypomorphic cartilage responded to loading by an expression signature of negative regulation of apoptosis with pro-apoptotic Bnip3 being selectively down-regulated. HS-deficiency enhanced BMP-sensitivity, GAG-production and fostered an anti-apoptotic expression signature after loading, all of which may protect cartilage from load-induced erosion.

scholarly journals Multi-omics analysis reveals contextual tumor suppressive and oncogenic gene modules within the acute hypoxic response

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zdenek Andrysik ◽  
Heather Bender ◽  
Matthew D. Galbraith ◽  
Joaquin M. Espinosa
Keyword(s):  
Cancer Biology ◽  
Acute Hypoxia ◽  
Transcriptional Response ◽  
Adaptation To Hypoxia ◽  
Mtor Inhibition ◽  
Collagen Remodeling ◽  
Acute Response ◽  
Relative Contribution ◽  
Transcriptional Changes ◽  
Cancer Types

AbstractCellular adaptation to hypoxia is a hallmark of cancer, but the relative contribution of hypoxia-inducible factors (HIFs) versus other oxygen sensors to tumorigenesis is unclear. We employ a multi-omics pipeline including measurements of nascent RNA to characterize transcriptional changes upon acute hypoxia. We identify an immediate early transcriptional response that is strongly dependent on HIF1A and the kinase activity of its cofactor CDK8, includes indirect repression of MYC targets, and is highly conserved across cancer types. HIF1A drives this acute response via conserved high-occupancy enhancers. Genetic screen data indicates that, in normoxia, HIF1A displays strong cell-autonomous tumor suppressive effects through a gene module mediating mTOR inhibition. Conversely, in advanced malignancies, expression of a module of HIF1A targets involved in collagen remodeling is associated with poor prognosis across diverse cancer types. In this work, we provide a valuable resource for investigating context-dependent roles of HIF1A and its targets in cancer biology.

scholarly journals Transcriptional Changes in Potato Sprouts upon Interaction with Rhizoctonia solani Indicate Pathogen-Induced Interference in the Defence Pathways of Potato

2021 ◽  
Vol 22 (6) ◽  
pp. 3094
Author(s):  
Rita Zrenner ◽  
Bart Verwaaijen ◽  
Franziska Genzel ◽  
Burkhardt Flemer ◽  
Rita Grosch
Keyword(s):  
Rhizoctonia Solani ◽  
Rna Sequencing ◽  
Control Strategies ◽  
Transcriptional Response ◽  
Black Scurf ◽  
Post Inoculation ◽  
Molecular Response ◽  
Resistance Level ◽  
Sequencing Experiment ◽  
Transcriptional Changes

Rhizoctonia solani is the causer of black scurf disease on potatoes and is responsible for high economical losses in global agriculture. In order to increase the limited knowledge of the plants’ molecular response to this pathogen, we inoculated potatoes with R. solani AG3-PT isolate Ben3 and carried out RNA sequencing with total RNA extracted from potato sprouts at three and eight days post inoculation (dpi). In this dual RNA-sequencing experiment, the necrotrophic lifestyle of R. solani AG3-PT during early phases of interaction with its host has already been characterised. Here the potato plants’ comprehensive transcriptional response to inoculation with R. solani AG3 was evaluated for the first time based on significantly different expressed plant genes extracted with DESeq analysis. Overall, 1640 genes were differentially expressed, comparing control (−Rs) and with R. solani AG3-PT isolate Ben3 inoculated plants (+Rs). Genes involved in the production of anti-fungal proteins and secondary metabolites with antifungal properties were significantly up regulated upon inoculation with R. solani. Gene ontology (GO) terms involved in the regulation of hormone levels (i.e., ethylene (ET) and jasmonic acid (JA) at 3 dpi and salicylic acid (SA) and JA response pathways at 8 dpi) were significantly enriched. Contrastingly, the GO term “response to abiotic stimulus” was down regulated at both time points analysed. These results may support future breeding efforts toward the development of cultivars with higher resistance level to black scurf disease or the development of new control strategies.

scholarly journals ‘Candidatus Phytoplasma solani’ interferes with the distribution and uptake of iron in tomato

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Sara Buoso ◽  
Laura Pagliari ◽  
Rita Musetti ◽  
Marta Martini ◽  
Fabio Marroni ◽  
...  
Keyword(s):  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Transcriptional Response ◽  
Transcriptome Profiling ◽  
Transport Processes ◽  
Fe Deficiency ◽  
Cultivated Plants ◽  
Chlorophyll Metabolism ◽  
Wide Range ◽  
Phytoplasma Infection

Abstract Background ‘Candidatus Phytoplasma solani’ is endemic in Europe and infects a wide range of weeds and cultivated plants. Phytoplasmas are prokaryotic plant pathogens that colonize the sieve elements of their host plant, causing severe alterations in phloem function and impairment of assimilate translocation. Typical symptoms of infected plants include yellowing of leaves or shoots, leaf curling, and general stunting, but the molecular mechanisms underlying most of the reported changes remain largely enigmatic. To infer a possible involvement of Fe in the host-phytoplasma interaction, we investigated the effects of ‘Candidatus Phytoplasma solani’ infection on tomato plants (Solanum lycopersicum cv. Micro-Tom) grown under different Fe regimes. Results Both phytoplasma infection and Fe starvation led to the development of chlorotic leaves and altered thylakoid organization. In infected plants, Fe accumulated in phloem tissue, altering the local distribution of Fe. In infected plants, Fe starvation had additive effects on chlorophyll content and leaf chlorosis, suggesting that the two conditions affected the phenotypic readout via separate routes. To gain insights into the transcriptional response to phytoplasma infection, or Fe deficiency, transcriptome profiling was performed on midrib-enriched leaves. RNA-seq analysis revealed that both stress conditions altered the expression of a large (> 800) subset of common genes involved in photosynthetic light reactions, porphyrin / chlorophyll metabolism, and in flowering control. In Fe-deficient plants, phytoplasma infection perturbed the Fe deficiency response in roots, possibly by interference with the synthesis or transport of a promotive signal transmitted from the leaves to the roots. Conclusions ‘Candidatus Phytoplasma solani’ infection changes the Fe distribution in tomato leaves, affects the photosynthetic machinery and perturbs the orchestration of root-mediated transport processes by compromising shoot-to-root communication.

scholarly journals Role of the cytoskeleton in muscle transcriptional responses to altered use

2013 ◽  
Vol 45 (8) ◽  
pp. 321-331 ◽  
Author(s):  
Gretchen A. Meyer ◽  
Simon Schenk ◽  
Richard L. Lieber
Keyword(s):  
Mechanical Response ◽  
Fiber Type ◽  
Transcriptional Response ◽  
Primary Component ◽  
Transcriptional Responses ◽  
Expression Of Genes ◽  
Elevated Expression ◽  
Transcriptional Changes ◽  
Type Shift ◽  
Future Work

In this work, the interaction between the loss of a primary component of the skeletal muscle cytoskeleton, desmin, and two common physiological stressors, acute mechanical injury and aging, were investigated at the transcriptional, protein, and whole muscle levels. The transcriptional response of desmin knockout ( des −/−) plantarflexors to a bout of 50 eccentric contractions (ECCs) showed substantial overlap with the response in wild-type ( wt) muscle. However, changes in the expression of genes involved in muscle response to injury were blunted in adult des −/− muscle compared with wt (fold change with ECC in des −/− and wt, respectively: Mybph, 1.4 and 2.9; Xirp1, 2.2 and 5.7; Csrp3, 1.8 and 4.3), similar to the observed blunted mechanical response (torque drop: des −/− 30.3% and wt 55.5%). Interestingly, in the absence of stressors, des −/− muscle exhibited elevated expression of many these genes compared with wt. The largest transcriptional changes were observed in the interaction between aging and the absence of desmin, including many genes related to slow fiber pathway (Myh7, Myl3, Atp2a2, and Casq2) and insulin sensitivity (Tlr4, Trib3, Pdk3, and Pdk4). Consistent with these transcriptional changes, adult des −/− muscle exhibited a significant fiber type shift from fast to slow isoforms of myosin heavy chain ( wt, 5.3% IIa and 71.7% IIb; des −/−, 8.4% IIa and 61.4% IIb) and a decreased insulin-stimulated glucose uptake ( wt, 0.188 μmol/g muscle/20 min; des −/−, 0.085 μmol/g muscle/20 min). This work points to novel areas of influence of this cytoskeletal protein and directs future work to elucidate its function.

Aldosterone-stimulated PKC signalling cascades: from receptor to effector

2007 ◽  
Vol 35 (5) ◽  
pp. 1049-1051 ◽  
Author(s):  
W. Thomas ◽  
V. McEneaney ◽  
B.J. Harvey
Keyword(s):  
Protein Kinase ◽  
Growth Factor Receptor ◽  
Transcriptional Response ◽  
Protein Kinase D ◽  
Cell Trafficking ◽  
Signalling Cascades ◽  
Transcriptional Changes ◽  
Epidermal Growth ◽  
Protein Kinase Signalling ◽  
Regulation Of Blood Pressure

Aldosterone plays an important role in the regulation of blood pressure. The effects of this hormone have classically been described in terms of the transcriptional regulation of genes that facilitate electrolyte transport, particularly across high-resistance epithelia. The protein kinase signalling cascades that are rapidly activated in response to aldosterone are emerging as important modulators of the transcriptional response, and may serve to prime cells for the subsequent transcriptional changes. The activation of protein kinase D through an epidermal growth factor receptor transactivation pathway by aldosterone in renal cells has the potential to impact on cell trafficking events that regulate transporter activity.

scholarly journals Mechanism of Hypoxia-Induced NF-κB

2010 ◽  
Vol 30 (20) ◽  
pp. 4901-4921 ◽  
Author(s):  
Carolyn Culver ◽  
Anders Sundqvist ◽  
Sharon Mudie ◽  
Andrew Melvin ◽  
Dimitris Xirodimas ◽  
...  
Keyword(s):  
Target Genes ◽  
Physiological Role ◽  
Transcriptional Response ◽  
Conjugation System ◽  
Ubiquitin Chain ◽  
Calcium Calmodulin Dependent ◽  
Hypoxic Conditions ◽  
Iκb Kinase ◽  
Sumo Proteases ◽  
Underlying Mechanisms

ABSTRACT NF-κB activation is a critical component in the transcriptional response to hypoxia. However, the underlying mechanisms that control its activity under these conditions are unknown. Here we report that under hypoxic conditions, IκB kinase (IKK) activity is induced through a calcium/calmodulin-dependent kinase 2 (CaMK2)-dependent pathway distinct from that for other common inducers of NF-κB. This process still requires IKK and the IKK kinase TAK1, like that for inflammatory inducers of NF-κB, but the TAK1-associated proteins TAB1 and TAB2 are not essential. IKK complex activation following hypoxia requires Ubc13 but not the recently identified LUBAC (linear ubiquitin chain assembly complex) ubiquitin conjugation system. In contrast to the action of other NF-κB inducers, IKK-mediated phosphorylation of IκBα does not result in its degradation. We show that this results from IκBα sumoylation by Sumo-2/3 on critical lysine residues, normally required for K-48-linked polyubiquitination. Furthermore, inhibition of specific Sumo proteases is sufficient to release RelA from IκBα and activate NF-κB target genes. These results define a novel pathway regulating NF-κB activation, important to its physiological role in human health and disease.

scholarly journals Probing the Unknowns in Cytokinin-Mediated Immune Defense in Arabidopsis with Systems Biology Approaches

2014 ◽  
Vol 8 ◽  
pp. BBI.S13462 ◽  
Author(s):  
Muhammad Naseem ◽  
Meik Kunz ◽  
Thomas Dandekar
Keyword(s):  
Systems Biology ◽  
Immune Responses ◽  
Protein Interactions ◽  
Immune Defense ◽  
Immune Functions ◽  
Protein Protein Interactions ◽  
Cytokinin Signaling ◽  
Host Immune Responses ◽  
Arabidopsis Protein ◽  
Underlying Mechanisms

Plant hormones involving salicylic acid (SA), jasmonic acid (JA), ethylene (Et), and auxin, gibberellins, and abscisic acid (ABA) are known to regulate host immune responses. However, plant hormone cytokinin has the potential to modulate defense signaling including SA and JA. It promotes plant pathogen and herbivore resistance; underlying mechanisms are still unknown. Using systems biology approaches, we unravel hub points of immune interaction mediated by cytokinin signaling in Arabidopsis. High-confidence Arabidopsis protein—protein interactions (PPI) are coupled to changes in cytokinin-mediated gene expression. Nodes of the cellular interactome that are enriched in immune functions also reconstitute sub-networks. Topological analyses and their specific immunological relevance lead to the identification of functional hubs in cellular interactome. We discuss our identified immune hubs in light of an emerging model of cytokinin-mediated immune defense against pathogen infection in plants.

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