scholarly journals Deviating from the Beaten Track: New Twists in Brassinosteroid Receptor Function

2020 ◽  
Vol 21 (5) ◽  
pp. 1561 ◽  
Author(s):  
Sebastian Wolf
Keyword(s):  
Conceptual Models ◽  
Signalling Pathways ◽  
Environmental Cues ◽  
Receptor Complex ◽  
Environmental Signals ◽  
Surface Receptors ◽  
The Core ◽  
Beaten Track ◽  
Multiple Levels ◽  
New Evidence

A key feature of plants is their plastic development tailored to the environmental conditions. To integrate environmental signals with genetic growth regulatory programs, plants rely on a number of hormonal pathways, which are intimately connected at multiple levels. Brassinosteroids (BRs), a class of plant sterol hormones, are perceived by cell surface receptors and trigger responses instrumental in tailoring developmental programs to environmental cues. Arguably, BR signalling is one of the best-characterized plant signalling pathways, and the molecular composition of the core signal transduction cascade seems clear. However, BR research continues to reveal new twists to re-shape our view on this key signalling circuit. Here, exciting novel findings pointing to the plasma membrane as a key site for BR signalling modulation and integration with other pathways are reviewed and new inputs into the BR signalling pathway and emerging “non-canonical” functions of the BR receptor complex are highlighted. Together, this new evidence underscores the complexity of plant signalling integration and serves as a reminder that highly-interconnected signalling pathways frequently comprise non-linear aspects which are difficult to convey in classical conceptual models.

scholarly journals Signalling in Neutrophils: A Retro Look

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Paul H. Naccache
Keyword(s):  
Tyrosine Kinases ◽  
Second Messengers ◽  
Biological Properties ◽  
Present Knowledge ◽  
Polymorphonuclear Neutrophils ◽  
Signalling Pathways ◽  
Surface Receptors ◽  
The Core ◽  
Kinase C ◽  
Functional Responsiveness

This review presents a summary of signalling events related to the activation of human polymorphonuclear neutrophils by a variety of soluble and particulate agonists. It is not intended as a comprehensive review of this vast field or as a presentation of the multiple new aspects of neutrophil functions that are being documented at an ever faster rate. Its aim is rather to focus on multiple aspects of major signalling pathways that, in the view of this reviewer, are currently shadowed by present trends and to provide the core evidence for their implication and the limitations of our present knowledge. More specifically, this review starts with cell surface receptors and some of their functional and biological properties and then moves on to downstream transducers (G proteins) and effectors (the phosphoinositide, tyrosine kinases, and cyclic nucleotide pathways). Classical second messengers (calcium, protein kinase C, polyphosphoinositides, and cyclic nucleotides) are emphasized. It is hoped that this presentation will not only remind present-day investigators of the central role these pathways play in the regulation of the functional responsiveness of neutrophils, but that it will also highlight some of the areas deserving additional investigation.

scholarly journals Combinatorial Control of Gene Expression

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Soumya Bhattacharjee ◽  
Kaushik Renganaath ◽  
Rajesh Mehrotra ◽  
Sandhya Mehrotra
Keyword(s):  
Gene Expression ◽  
Short Description ◽  
Controlling Factors ◽  
Environmental Cues ◽  
Control Of Gene Expression ◽  
Environmental Signals ◽  
Combinatorial Control ◽  
Sense And Respond ◽  
Eukaryotic Organisms

The complexity and diversity of eukaryotic organisms are a feat of nature’s engineering. Pulling the strings of such an intricate machinery requires an even more masterful and crafty approach. Only the number and type of responses that they generate exceed the staggering proportions of environmental signals perceived and processed by eukaryotes. Hence, at first glance, the cell’s sparse stockpile of controlling factors does not seem remotely adequate to carry out this response. The question as to how eukaryotes sense and respond to environmental cues has no single answer. It is an amalgamation, an interplay between several processes, pathways, and factors—a combinatorial control. A short description of some of the most important elements that operate this entire conglomerate is given in this paper.

scholarly journals Cyclicity and Connectivity in Nez Perce Relative Clauses

2016 ◽  
Vol 47 (3) ◽  
pp. 427-470 ◽  
Author(s):  
Amy Rose Deal
Keyword(s):  
Word Order ◽  
Relative Clause ◽  
Crucial Role ◽  
Relative Clauses ◽  
Head Noun ◽  
Intermediate Position ◽  
Nez Perce ◽  
The Core ◽  
New Evidence ◽  
Relative Pronouns

This article studies two aspects of movement in relative clauses, focusing on evidence from Nez Perce. First, I argue that relativization involves cyclic Ā-movement, even in monoclausal relatives: the relative operator moves to Spec,CP via an intermediate position in an Ā outer specifier of TP. The core arguments draw on word order, complementizer choice, and a pattern of case attraction for relative pronouns. Ā cyclicity of this type suggests that the TP sister of relative C constitutes a phase—a result whose implications extend to an ill-understood corner of the English that-trace effect. Second, I argue that Nez Perce relativization provides new evidence for an ambiguity thesis for relative clauses, according to which some but not all relatives are derived by head raising. The argument comes from connectivity and anticonnectivity in morphological case. A crucial role is played by a pattern of inverse case attraction, wherein the head noun surfaces in a case determined internal to the relative clause. These new data complement the range of existing arguments concerning head raising, which draw primarily on connectivity effects at the syntax-semantics interface.

scholarly journals Interactions Among mTORC, AMPK and SIRT A Computational Model for Cell Energy Balance and Metabolism

2020 ◽  
Author(s):  
Mehrshad Sadria ◽  
Anita T. Layton
Keyword(s):  
Energy Balance ◽  
Computational Model ◽  
Metabolic Stress ◽  
Cellular Aging ◽  
Signalling Pathways ◽  
Environmental Signals ◽  
Metabolic Signalling ◽  
The Face ◽  
Cell Energy ◽  
Salvage Pathways

Abstract BackgroundCells adapt their metabolism and activities in response to signals from their surroundings, and this ability is essential for their survival in the face of perturbations. In tissues a deficit of these mechanisms is commonly associated with cellular aging and diseases, such as cardiovascular disease, cancer, immune system decline, and neurological pathologies. Several proteins have been identified as being able to respond directly to energy, nutrient, and growth factor levels and stress stimuli in order to mediate adaptations in the cell. In particular, mTOR, AMPK, and sirtuins are known to play an essential role in the management of metabolic stress and energy balance in mammals.MethodsTo understand the complex interactions of these signalling pathways and environmental signals, and how those interactions may impact lifespan and health-span, we have developed a computational model of metabolic signalling pathways. Specifically, the model includes the insulin/IGF-1 pathway, which couples energy and nutrient abundance to the execution of cell growth and division, (ii) mTORC1 and the amino acid sensors such as sestrin, (iii) the Preiss-Handler and salvage pathways, which regulate the metabolism of NAD+ and the NAD+-consuming factor SIRT1, (iv) the energy sensor AMPK, and (v) transcription factors FOXO and PGC-1α.ResultsThe model simulates the interactions among key regulators such as Akt, mTORC1, AMPK, NAD+, and SIRT, and predicts their dynamics. Key findings include the clinically important role of PRAS40 and diet in mTORC1 inhibition, and a potential link between SIRT1-activating compounds and premature autophagy. Moreover, the model captures the exquisite interactions of leucine, sestrin2, and arginine, and the resulting signal to the mTORC1 pathway. These results can be leveraged in the development of novel treatment of cancers and other diseases.ConclusionsThis study presents a state-of-the-art computational model for investigating the interactions among signaling pathways and environmental stimuli in growth, ageing, metabolism, and diseases. The model can be used as an essential component to simulate gene manipulation, therapies (e.g., rapamycin and wortmannin), calorie restrictions, and chronic stress, and assess their functional implications on longevity and ageing‐related diseases.

Intracellular signalling

2020 ◽  
pp. 256-265
Author(s):  
R. Andres Floto
Keyword(s):  
Signal Transduction ◽  
Plasma Membrane ◽  
Cell Surface ◽  
Intracellular Signalling ◽  
Signalling Pathways ◽  
Molecular Processes ◽  
Surface Receptors ◽  
Intracellular Signalling Pathways ◽  
Transmission Of Information ◽  
Effective Transmission

This chapter outlines the general principles of intracellular signalling. Focusing on cell surface receptors, the requirements for effective transmission of information across the plasma membrane are outlined. The principal mechanisms utilized in mammalian signal transduction are described. For each, the pathological consequences of aberrant signalling and means by which pathways can be pharmacologically targeted are described in molecular terms. Intracellular signalling pathways permit the transmission and integration of information within cells. Mammalian receptor signalling relies on only a small number of distinct molecular processes which interact to determine cellular responses. Rapid advances in our knowledge of the mechanisms of intracellular signalling has greatly increased understanding of how cells function physiologically, how they malfunction pathologically, and how their behaviour might be manipulated therapeutically.

scholarly journals Aflatoxin Biosynthesis and Genetic Regulation: A Review

Toxins ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 150 ◽  
Author(s):  
Isaura Caceres ◽  
Anthony Al Khoury ◽  
Rhoda El Khoury ◽  
Sophie Lorber ◽  
Isabelle P. Oswald ◽  
...  
Keyword(s):  
Genetic Regulation ◽  
Aflatoxin Production ◽  
Toxin Production ◽  
Molecular Study ◽  
Fungal Species ◽  
Molecular Techniques ◽  
Environmental Signals ◽  
Effective Strategies ◽  
Global Environmental ◽  
New Evidence

The study of fungal species evolved radically with the development of molecular techniques and produced new evidence to understand specific fungal mechanisms such as the production of toxic secondary metabolites. Taking advantage of these technologies to improve food safety, the molecular study of toxinogenic species can help elucidate the mechanisms underlying toxin production and enable the development of new effective strategies to control fungal toxicity. Numerous studies have been made on genes involved in aflatoxin B1 (AFB1) production, one of the most hazardous carcinogenic toxins for humans and animals. The current review presents the roles of these different genes and their possible impact on AFB1 production. We focus on the toxinogenic strains Aspergillus flavus and A. parasiticus, primary contaminants and major producers of AFB1 in crops. However, genetic reports on A. nidulans are also included because of the capacity of this fungus to produce sterigmatocystin, the penultimate stable metabolite during AFB1 production. The aim of this review is to provide a general overview of the AFB1 enzymatic biosynthesis pathway and its link with the genes belonging to the AFB1 cluster. It also aims to illustrate the role of global environmental factors on aflatoxin production and the recent data that demonstrate an interconnection between genes regulated by these environmental signals and aflatoxin biosynthetic pathway.

scholarly journals Transmembrane features governing Fc receptor CD16A assembly with CD16A signaling adaptor molecules

2017 ◽  
Vol 114 (28) ◽  
pp. E5645-E5654 ◽  
Author(s):  
Alfonso Blázquez-Moreno ◽  
Soohyung Park ◽  
Wonpil Im ◽  
Melissa J. Call ◽  
Matthew E. Call ◽  
...  
Keyword(s):  
Surface Expression ◽  
Site Directed Mutagenesis ◽  
Solution Nmr ◽  
Receptor Complex ◽  
Hydrogen Bond Network ◽  
The Core ◽  
High Sequence Homology ◽  
Bond Network ◽  
Tm Domain ◽  
Signaling Modules

Many activating immunoreceptors associate with signaling adaptor molecules like FcεR1γ or CD247. FcεR1γ and CD247 share high sequence homology and form disulphide-linked homodimers that contain a pair of acidic aspartic acid residues in their transmembrane (TM) domains that mediate assembly, via interaction with an arginine residue at a similar register to these aspartic acids, with the activating immunoreceptors. However, this model cannot hold true for receptors like CD16A, whose TM domains do not contain basic residues. We have carried out an extensive site-directed mutagenesis analysis of the CD16A receptor complex and now report that the association of receptor with the signaling adaptor depends on a network of polar and aromatic residues along the length of the TM domain. Molecular modeling indicates that CD16A TM residues F202, D205, and T206 form the core of the membrane-embedded trimeric interface by establishing highly favorable contacts to the signaling modules through rearrangement of a hydrogen bond network previously identified in the CD247 TM dimer solution NMR structure. Strikingly, the amino acid D205 also regulates the turnover and surface expression of CD16A in the absence of FcεR1γ or CD247. Modeling studies indicate that similar features underlie the association of other activating immune receptors, including CD64 and FcεR1α, with signaling adaptor molecules, and we confirm experimentally that equivalent F, D, and T residues in the TM domain of FcεR1α markedly influence the biology of this receptor and its association with FcεR1γ.

scholarly journals BdlA, a Chemotaxis Regulator Essential for Biofilm Dispersion in Pseudomonas aeruginosa

2006 ◽  
Vol 188 (21) ◽  
pp. 7335-7343 ◽  
Author(s):  
Ryan Morgan ◽  
Steven Kohn ◽  
Sung-Hei Hwang ◽  
Daniel J. Hassett ◽  
Karin Sauer
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Gene Product ◽  
Signaling Cascade ◽  
Environmental Cues ◽  
Environmental Sensing ◽  
Environmental Signals ◽  
Isogenic Mutant ◽  
Biofilm Detachment ◽  
Biofilm Dispersion ◽  
Do So

ABSTRACT Multiple environmental cues have been shown to trigger biofilm detachment, the transition from surface-attached, highly organized communities known as biofilms to the motile lifestyle. The goal of this study was to identify a gene product involved in sensing environmental cues that trigger biofilm dispersion in Pseudomonas aeruginosa. To do so, we focused on novel putative chemotaxis transducer proteins that could potentially be involved in environmental sensing. We identified a locus encoding such a protein that played a role in detachment, as indicated by the observation that an isogenic mutant biofilm could not disperse in response to a variety of environmental cues. The locus was termed bdlA for biofilm dispersion locus. The BdlA protein harbors an MCP (methyl-accepting chemotaxis protein) domain and two PAS (Per-Arnt-Sint) domains that have been shown to be essential for responding to environmental signals in other proteins. The dispersion-deficient phenotype of the bdlA mutant was confirmed by treatment with the biocide H2O2 and by microscopic observations. The dispersion response was independent of motility. bdlA mutant biofilms were found to have increased adherent properties and increased intracellular levels of cyclic di-GMP (c-di-GMP). Our findings suggest that BdlA may be a link between sensing environmental cues, c-di-GMP levels, and detachment. Based on our findings, a possible involvement of BdlA in a signaling cascade resulting in biofilm dispersion is discussed.

scholarly journals Kinetic analysis of internalization, recycling and redistribution of atrial natriuretic factor-receptor complex in cultured vascular smooth-muscle cells. Ligand-dependent receptor down-regulation

1992 ◽  
Vol 288 (1) ◽  
pp. 55-61 ◽  
Author(s):  
K N Pandey
Keyword(s):  
Smooth Muscle ◽  
Cell Surface ◽  
Atrial Natriuretic Factor ◽  
Dependent Manner ◽  
Receptor Complex ◽  
Down Regulation ◽  
Surface Receptors ◽  
Natriuretic Factor ◽  
Metabolic Degradation ◽  
Atrial Natriuretic

The kinetics of internalization, sequestration and metabolic degradation of atrial natriuretic factor (ANF)-receptor complex were studied in rat thoracic aortic smooth-muscle (RTASM) cells. These parameters were directly determined by measuring 125I-ANF binding to total, intracellular and cell-surface receptors. Pretreatment of cells with the lysosomotropic agent chloroquine and the energy depleter dinitrophenol led to an increase in the intracellular 125I-ANF radioactivity. After 60 min incubation at 37 degrees C, cell-associated 125I-ANF radioactivity fell rapidly in chloroquine-treated cells (> 85%) compared with the controls (< 45%). 125I-ANF radioactivity increased to a peak of 65% of the initial level within 15 min in chloroquine-treated cells compared with only 22% in the control cells. During the initial incubation period at 37 degrees C, chloroquine inhibited the release of both intact and degraded 125I-ANF in a time-dependent manner. However, at later incubation times, the effect of chloroquine was diminished and release of both degraded and intact ligand was resumed. Extracellular unlabelled ANF did not affect the release of degraded 125I-ANF but it accelerated the release of intact ANF by a retroendocytotic mechanism. After the endocytosis, about 30-40% of ANF receptors were restored to the cell surface from the internalized pool of receptors. The restoration was blocked by chloroquine or dinitrophenol but not by cycloheximide. Exposure of RTASM cells to unlabelled ANF resulted in a time- and concentration-dependent loss of ANF receptors. Unlabelled ANF (10 nM) induced a loss of more than 52% of 125I-ANF binding, and a complete loss occurred at micromolar concentrations. It is inferred that ANF-induced down-regulation of its receptor resulted primarily from an increased rate in internalization and metabolic degradation of ligand-receptor complex by receptor-mediated endocytotic mechanisms.

PECAM-1 functions as a specific and potent inhibitor of mitochondrial-dependent apoptosis

Blood ◽  
2003 ◽  
Vol 102 (1) ◽  
pp. 169-179 ◽  
Author(s):  
Cunji Gao ◽  
Weiyong Sun ◽  
Melpo Christofidou-Solomidou ◽  
Motoshi Sawada ◽  
Debra K. Newman ◽  
...  
Keyword(s):  
Cell Surface ◽  
Immunoglobulin Gene ◽  
Vascular Cells ◽  
Cytochrome C Release ◽  
Homophilic Binding ◽  
Environmental Signals ◽  
Surface Receptors ◽  
Naturally Occurring ◽  
Platelet Endothelial Cell Adhesion ◽  
Cell Adhesion Molecule 1

Abstract Programmed cell death, or apoptosis, is a tightly regulated, naturally occurring process by which damaged or unwanted cells are removed. Dysregulated apoptosis has been implicated in a variety of pathophysiological conditions, including degenerative diseases, tissue remodeling, and tumorogenesis. The decision to live or die results from integration of numerous environmental signals transmitted by specific classes of cell surface receptors that bind hormones, growth factors, or components of the extracellular matrix. Here we show that platelet endothelial cell adhesion molecule-1 (PECAM-1), a homophilic-binding member of the immunoreceptor tyrosine-based inhibitory motif (ITIM) family of inhibitory receptors, functions prominently to inhibit apoptosis in naturally occurring vascular cells subjected to apoptotic stimuli. Murine endothelial cells and human T lymphocytes lacking PECAM-1 were found to be far more sensitive than their PECAM-1—expressing counterparts to multiple death signals that stimulate Bax, a multidomain, proapoptotic member of the Bcl-2 family that plays a central role in mitochondrial dysfunction-dependent apoptosis. In addition, PECAM-1 markedly suppressed Bax overexpression—induced cytochrome c release, caspase activation, and nuclear fragmentation. Amino acid substitutions within PECAM-1's extracellular homophilic binding domain, or within its cytoplasmic ITIM, completely abolished PECAM-1—mediated cytoprotection. Taken together, these data implicate PECAM-1 as a novel and potent suppressor of Bax-mediated apoptosis and suggest that members of the immunoglobulin gene (Ig) superfamily, like cell surface integrins, may also transmit survival signals into blood and vascular cells. (Blood. 2003;102:169-179)

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