Cellular mechanisms of callose deposition in response to fungal infection or chemical damage

1996 ◽  
Vol 74 (8) ◽  
pp. 1236-1242 ◽  
Author(s):  
Dubravka Škalamera ◽  
Michèle C. Heath
Keyword(s):  
Protein Synthesis ◽  
Boric Acid ◽  
Rust Fungus ◽  
Brefeldin A ◽  
Protein Glycosylation ◽  
Cellular Mechanisms ◽  
Callose Deposition ◽  
Cellular Processes ◽  
Microtubule Polymerization ◽  
Chemical Inhibitors

Cellular mechanisms of callose deposition induced in cowpea (Vigna unguiculata) leaves by the living cowpea rust fungus (Uromyces vignae), boric acid, or the fungus killed by polyoxin D, were investigated by the use of chemical inhibitors. Effects of the inhibitors were observed in both a resistant and a susceptible cowpea cultivar. The effect of inhibitors differed depending on the type of callose-inducing stimulus and cultivar used. Inhibitors of transcription (actinomycin D) and protein synthesis (blasticidin S, cycloheximide) lowered the incidence of fungus-induced callose deposits in both cultivars. Inhibitors of protein synthesis also reduced deposits induced by boric acid or fungal death. Callose deposition induced by the living fungus in the resistant cultivar was reduced by inhibitors of protein glycosylation (tunicamycin, deoxynojirimycin) and microfilament function (cytochalasins B and E), but these inhibitors had no effect on callose deposition in the susceptible cultivar or on chemical or fungal death-induced deposition in either cultivar. No reduction in callose deposits was observed in plants treated with inhibitors of Golgi-associated vesicle transfer (brefeldin A, monensin) or microtubule polymerization (colchicine, oryzalin). The results suggest that the cellular processes involved in callose deposition differ with differing triggering stimuli and that callose deposition triggered by the living fungus in a resistant host cultivar is not a typical wound or damage response. Keywords: callose, infection, inhibitors, resistance, rust fungi.

scholarly journals Mechanisms of Lifespan Extension by Sirt6 in Drosophila melanogaster

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 736-736
Author(s):  
Jackson Taylor ◽  
Jason Wood ◽  
Matthew Finn ◽  
Julianna Liu ◽  
Evan Mizerak ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Drosophila Melanogaster ◽  
Target Genes ◽  
Molecular Regulation ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Short Lifespan ◽  
Expression Of Genes ◽  
Median Lifespan ◽  
Biochemical Analyses

Abstract Sirt6 is a multifunctional enzyme that regulates numerous cellular processes connected to longevity. Overexpressing Sirt6 extends lifespan in mice, but the underlying cellular mechanisms are unclear. Here, we used the powerful genetic tools and short lifespan of Drosophila melanogaster to better understand the precise mechanisms by which Sirt6 regulates longevity. Sirt6 OE in flies produces robust extension of median lifespan in both sexes. Molecular and biochemical analyses reveal that Sirt6 OE reduces expression of genes involved in protein synthesis, including many Myc target genes, via epigenetic regulation. We will further discuss our findings on the connection between Sirt6, Myc, and the molecular regulation of protein synthesis and lifespan, as well as additional Sirt6 longevity mechanisms we identified, including autophagy and silencing of transposable elements.

Inhibition of atrial peptide secretion at different stages of the secretory process: Ca2+ dependence

1991 ◽  
Vol 261 (6) ◽  
pp. C1162-C1172 ◽  
Author(s):  
E. Page ◽  
J. Upshaw-Earley ◽  
G. E. Goings ◽  
D. A. Hanck
Keyword(s):  
Protein Synthesis ◽  
Brefeldin A ◽  
Atp Depletion ◽  
Secretory Process ◽  
Protein Synthesis Inhibitors ◽  
Large Reservoir ◽  
Secretory Rate ◽  
Vesicular Traffic ◽  
Dependent Inactivation

We have used a noncontracting in vitro preparation of stretched and unstretched rat atria to estimate contributions of constitutive and regulated pathways to the rates of stretch-augmented and basal secretion of immunoreactive atrial natriuretic peptide (ANP) and to examine effects of inhibition of the secretory sequence by 1) protein synthesis inhibitors, 2) disruption of forward vesicular traffic between endoplasmic reticulum and Golgi with brefeldin A (BFA, and 3) cellular ATP depletion. Protein synthesis inhibition with cycloheximide for 44 min slowed neither basal nor stretch-augmented ANP secretion but instead accelerated stretch-augmented secretion at low (but not at physiological) external Ca2+ concentration, suggesting that the constitutive component does not contribute substantially to either basal or stretch-augmented secretion. BFA, which disassembled Golgi cisternae, increased the stretch-augmented secretory rate via the regulated pathway and prevented Ca(2+)-dependent inactivation with time. Cellular ATP depletion rapidly and completely inhibited stretch-augmented secretion. We conclude that both basal and stretch-augmented utilize the energy-dependent regulated pathway, drawing on a large reservoir of concentrated prohormone stored in granules that is not detectably depleted during 44 min of stretch-augmented secretion at 37 degrees C.

scholarly journals Maternal Uterine Vascular Remodeling During Pregnancy

Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala
Keyword(s):  
Extracellular Matrix ◽  
Blood Flow ◽  
Vascular Remodeling ◽  
Normal Pregnancy ◽  
Uterine Blood Flow ◽  
Growth And Remodeling ◽  
Cellular Mechanisms ◽  
Cellular Processes ◽  
Uteroplacental Blood Flow ◽  
Uterine Circulation

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.

scholarly journals Fed-state clamp stimulates cellular mechanisms of muscle protein anabolism and modulates glucose disposal in normal men

2009 ◽  
Vol 296 (1) ◽  
pp. E105-E113 ◽  
Author(s):  
Olasunkanmi A. J. Adegoke ◽  
Stéphanie Chevalier ◽  
José A. Morais ◽  
Réjeanne Gougeon ◽  
Scot R. Kimball ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Translation Initiation ◽  
Muscle Protein ◽  
Whole Body ◽  
Glucose Disposal ◽  
Metabolic Clearance ◽  
Cellular Mechanisms ◽  
Body Protein ◽  
Fed State ◽  
Mtorc1 Signaling

Since maximum anabolism occurs postprandially, we developed a simulated fed state with clamped hyperinsulinemia, physiological hyperglycemia, and hyperaminoacidemia (Hyper-3) and explored muscle cellular mechanisms. Whole body [1-13C]leucine and [3-3H]glucose kinetics in healthy men were compared between hyperinsulinemic, euglycemic, isoaminoacidemic (Hyper-1, n = 10) and Hyper-3 ( n = 9) clamps. In Hyper-3 vs. Hyper-1, nonoxidative leucine Rd [rate of disappearance (synthesis)] was stimulated more (45 ± 4 vs. 24 ± 4 μmol/min, P < 0.01) and endogenous Ra [rate of appearance (breakdown)] was inhibited similarly; hence net balance increased more (86 ± 6 vs. 49 ± 2 μmol/min, P < 0.001). Glucose Rd was similar; thus Hyper-3 metabolic clearance rate (331 ± 23 vs. 557 ± 41 ml/min, P < 0.0005) and Rd/insulin (M, 0.65 ± 0.10 vs. 1.25 ± 0.10 mg·min−1·pmol−1·l, P < 0.001) were less, despite higher insulin (798 ± 74 vs. 450 ± 24 pmol/l, P < 0.005). In vastus lateralis muscle biopsies, phosphorylation of Akt ( P = 0.025), mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (p70S6K1; P = 0.008), S6 ( P = 0.049), and 4E-binding protein 1 (4E-BP1; P = 0.001) increased. With decreased eukaryotic initiation factor-4E (eIF4E)·4E-BP1 complex ( P = 0.01), these are consistent with increased mTOR complex 1 (mTORC1) signaling and translation initiation of protein synthesis. Although mRNA expression of ubiquitin, MAFbx 1, and MuRF-1 was unchanged, total ubiquitinated proteins decreased 20% ( P < 0.01), consistent with proteolysis suppression. The Hyper-3 clamp increases whole body protein synthesis, net anabolism, and muscle protein translation initiation pathways and decreases protein ubiquitination. The main contribution of hyperaminoacidemia is stimulation of synthesis rather than inhibition of proteolysis, and it attenuates the expected increment of glucose disposal.

The effects of inhibition of protein glycosylation on the aggregation of Dictyostelium discoideum

Development ◽  
1983 ◽  
Vol 78 (1) ◽  
pp. 229-248
Author(s):  
Charles John McDonald ◽  
Jeffrey Sampson
Keyword(s):  
Protein Synthesis ◽  
Cyclic Amp ◽  
Cell Surface ◽  
Dictyostelium Discoideum ◽  
Total Protein ◽  
Subsequent Development ◽  
Protein Glycosylation ◽  
Normal Process ◽  
Contact Sites ◽  
Cyclic Amp Phosphodiesterase

At concentrations greater than 10 µg ml−1 tunicamycin inhibited the incorporation of [3H]mannose into glycoproteins during the early phase of development in Dictyostelium discoideum, however, total protein synthesis was unaffected. Tunicamycin also interfered with the normal process of aggregation. In its presence small aggregates were observed at the time of normal aggregation, but amoebae failed to aggregate completely and subsequent development was inhibited. Inhibition of normal aggregation by tunicamycin was found to be reversible. The appearance of cell-associated and secreted cyclic AMP phosphodiesterase and cell-surface contact sites A was prevented by tunicamycin but cell surface cyclic AMP receptor activity developed normally in its presence. Tunicamycin also prevented amoebae from acquiring the ability to chemotact toward cyclic AMP. Addition of exogenous cyclic AMP phosphodiesterase restored the ability of amoebae to chemotact toward cyclic AMP in the presence of tunicamycin. Our data suggest that the primary block in aggregation caused by tunicamycin results from the inhibition of expression of active cyclic AMP phosphodiesterase.

Abstract 497: Cholesterol and Toll-like Receptor Signaling Are Important Regulators of Macrophage Interactions with Atherosclerotic Lipoprotein Aggregates

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Harvey F Chin ◽  
Abigail Haka ◽  
Frederick R Maxfield
Keyword(s):  
Molecular Mechanisms ◽  
Atherosclerotic Plaques ◽  
Cholesteryl Esters ◽  
Cellular Mechanisms ◽  
Downstream Signaling ◽  
Cellular Processes ◽  
Atherosclerotic Plaque Formation ◽  
Subendothelial Space ◽  
Morphological Responses ◽  
Cytoskeletal Rearrangements

Macrophages encounter deposits of aggregated low-density lipoproteins (agLDL) in the subendothelial space of blood vessels during the first stages of atherosclerotic plaque formation. Notably, current models for the mechanism of macrophage internalization of cholesterol in early atherosclerotic plaques are incomplete due to the lack of attention paid to the unique cellular mechanisms that are required for macrophages to degrade aggregates of LDL in particular, which can comprise >90% of the LDL in atherosclerotic plaques. In fact, internalization of cholesterol from cholesteryl esters in agLDL involves the development of intriguing cellular processes in which extracellular acidic compartments, lysosomal synapses (LSs), are formed whereby agLDL is partially degraded prior to internalization. This process requires extensive cytoskeletal rearrangements and secretion of lysosomal enzymes responsible for hydrolysis of cholesteryl esters from the agLDL. Subsequent delivery of free cholesterol from agLDL to the macrophage plasma membrane is central for development of the LS. Nonetheless, the molecular mechanism underlying initiation and propagation of the LS are currently largely unknown. This research proposal aims to elucidate the molecular mechanisms of LS formation and the role that cholesterol plays in eliciting these morphological responses to agLDL. Fluorescence microscopy assays were used to identify activation of TLR4 and downstream signaling involving PI3K and Akt as important events leading to LS formation. Furthermore, morphological responses of macrophages to cholesterol overloading require overlapping signaling pathways, indicating the role of interplay of cholesterol and TLR4 signaling in development of this novel macrophage interaction with aggregated LDL found in plaques. Identification of specific molecular pathways involved in this process will not only contribute to the basic understanding of one of the primary cellular processes contributing to atherosclerosis, one of the primary causes of heart disease, but also provide tangible molecular targets for the ultimate development of therapies.

scholarly journals Tyrosine phosphorylation of the scaffold protein IQGAP1 in the MET pathway alters function

2020 ◽  
Vol 295 (52) ◽  
pp. 18105-18121
Author(s):  
Andrew C. Hedman ◽  
Dean E. McNulty ◽  
Zhigang Li ◽  
Laëtitia Gorisse ◽  
Roland S. Annan ◽  
...  
Keyword(s):  
Cell Function ◽  
Scaffold Protein ◽  
Site Directed Mutagenesis ◽  
Human Lung Cancer ◽  
Post Translational Modifications ◽  
Akt Activation ◽  
Cellular Processes ◽  
Src Signaling ◽  
Chemical Inhibitors ◽  
Hepatocyte Growth

IQGAP1 is a key scaffold protein that regulates numerous cellular processes and signaling pathways. Analogous to many other cellular proteins, IQGAP1 undergoes post-translational modifications, including phosphorylation. Nevertheless, very little is known about the specific sites of phosphorylation or the effects on IQGAP1 function. Here, using several approaches, including MS, site-directed mutagenesis, siRNA-mediated gene silencing, and chemical inhibitors, we identified the specific tyrosine residues that are phosphorylated on IQGAP1 and evaluated the effect on function. Tyr-172, Tyr-654, Tyr-855, and Tyr-1510 were phosphorylated on IQGAP1 when phosphotyrosine phosphatase activity was inhibited in cells. IQGAP1 was phosphorylated exclusively on Tyr-1510 under conditions with enhanced MET or c-Src signaling, including in human lung cancer cell lines. This phosphorylation was significantly reduced by chemical inhibitors of MET or c-Src or by siRNA-mediated knockdown of MET. To investigate the biological sequelae of phosphorylation, we generated a nonphosphorylatable IQGAP1 construct by replacing Tyr-1510 with alanine. The ability of hepatocyte growth factor, the ligand for MET, to promote AKT activation and cell migration was significantly greater when IQGAP1-null cells were reconstituted with IQGAP1 Y1510A than when cells were reconstituted with WT IQGAP1. Collectively, our data suggest that phosphorylation of Tyr-1510 of IQGAP1 alters cell function. Because increased MET signaling is implicated in the development and progression of several types of carcinoma, IQGAP1 may be a potential therapeutic target in selected malignancies.

scholarly journals Molecular and Clinical Insights into the Invasive Capacity of Glioblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Carlos Velásquez ◽  
Sheila Mansouri ◽  
Carla Mora ◽  
Farshad Nassiri ◽  
Suganth Suppiah ◽  
...  
Keyword(s):  
Treatment Resistance ◽  
Host Cells ◽  
Cellular Mechanisms ◽  
Poor Overall Survival ◽  
Cellular Processes ◽  
New Therapeutic Approaches ◽  
Invasive Capacity ◽  
Molecular Machinery ◽  
The Impact ◽  
Infiltrative Tumor

The invasive capacity of GBM is one of the key tumoral features associated with treatment resistance, recurrence, and poor overall survival. The molecular machinery underlying GBM invasiveness comprises an intricate network of signaling pathways and interactions with the extracellular matrix and host cells. Among them, PI3k/Akt, Wnt, Hedgehog, and NFkB play a crucial role in the cellular processes related to invasion. A better understanding of these pathways could potentially help in developing new therapeutic approaches with better outcomes. Nevertheless, despite significant advances made over the last decade on these molecular and cellular mechanisms, they have not been translated into the clinical practice. Moreover, targeting the infiltrative tumor and its significance regarding outcome is still a major clinical challenge. For instance, the pre- and intraoperative methods used to identify the infiltrative tumor are limited when trying to accurately define the tumor boundaries and the burden of tumor cells in the infiltrated parenchyma. Besides, the impact of treating the infiltrative tumor remains unclear. Here we aim to highlight the molecular and clinical hallmarks of invasion in GBM.

Non-host resistance responses of Arabidopsis thaliana to the coffee leaf rust fungus (Hemileia vastatrix)

Botany ◽  
2010 ◽  
Vol 88 (7) ◽  
pp. 621-629 ◽  
Author(s):  
Helena Gil Azinheira ◽  
Maria do Céu Silva ◽  
Pedro Talhinhas ◽  
Clara Medeira ◽  
Isabel Maia ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Leaf Rust ◽  
Rust Fungus ◽  
Hemileia Vastatrix ◽  
Callose Deposition ◽  
Mesophyll Cells ◽  
Model Plant ◽  
Heterologous System ◽  
Coffee Leaf Rust ◽  
Model Plant Arabidopsis Thaliana

Leaf rust, caused by Hemileia vastatrix Berk & Broome, is the most destructive fungal disease of coffee. In the absence of a suitable gene validation system in coffee, the objective of this study was to investigate whether the model plant Arabidopsis thaliana (L.) Heynh. may be used as a heterologous system for the molecular dissection of coffee responses to leaf rust. Histological examination of A. thaliana (Col-0) leaves inoculated with H. vastatrix (race II) showed that by 24 h after inoculation (hai), H. vastatrix uredospores differentiated appressoria and penetrated the stomata, but failed to form haustoria. Arabidopsis thaliana cellular resistance responses included hypersensitive-like response (HR) of stomata guard cells together with accumulation of phenolic compounds and callose deposition in walls of epidermal and mesophyll cells. Results indicate that H. vastatrix infection triggered the induction of a set of defence-related genes peaking at 18 and 42 hai. The non-host HR triggered by H. vastatrix in the model plant A. thaliana makes it usable to infer the function of coffee genes involved in pre-haustorial rust resistance.

Sign in / Sign up

Export Citation Format

Share Document