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LuxR Solos are Becoming Major Players in Cell-Cell Communication in Bacteria

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199174 Year: Pages: 122 DOI: 10.3389/978-2-88919-917-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology
Added to DOAB on : 2016-01-19 14:05:46
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The most common quorum sensing (QS) system in Gram-negative bacteria occurs via N-acyl homoserine lactone (AHLs) signals. An archetypical system consists of a LuxI-family protein synthesizing the AHL signal which binds at quorum concentrations to the cognate LuxR-family transcription factors which then control gene expression by binding to specific sequences in target gene promoters. QS LuxR-family proteins are approximately 250 amino acids long and made up of two domains; at the N-terminus there is an autoinducer-binding domain whereas the C-terminus contains a DNA-binding helix-turn-helix (HTH) domain. QS LuxRs display surprisingly low similarities (18-25%) even if they respond to structurally similar AHLs. 95% of LuxRs share 9 highly conserved amino acid residues; six of these are hydrophobic or aromatic and form the cavity of the AHL-binding domain and the remaining three are in the HTH domain. With only very few exceptions, the luxI/R cognate genes of AHL QS systems are located adjacent to each other. The sequencing of many bacterial genomes has revealed that many proteobacteria also possess LuxRs that do not have a cognate LuxI protein associated with them. These LuxRs have been called orphans and more recently solos. LuxR solos are widespread in proteobacterial species that possess a canonical complete AHL QS system as well as in species that do not. In many cases more than one LuxR solo is present in a bacterial genome. Scientists are beginning to investigate these solos. Are solos responding to AHL signals? If present in a bacterium which possesses a canonical AHL QS system are solos an integral part of the regulatory circuit? Are LuxR solos eavesdropping on AHLs produced by neighboring bacteria? Have they evolved to respond to different signals instead of AHLs, and are these signals endogenously produced or exogenously provided? Are they involved in interkingdom signaling by responding to eukaryotic signals? Recent studies have revealed that LuxR solos are involved in several mechanisms of cell-cell communication in bacteria implicating them in bacterial intraspecies and interspecies communication as well as in interkingdom signaling by responding to molecules produced by eukaryotes. LuxR solos are likely to become major players in signaling since they are widespread among proteobacterial genomes and because initial studies highlight their different roles in bacterial communication. This Research Topic allows scientists studying or interested in LuxR solos to report their data and/or express their hypotheses and thoughts on this important and currently understudied family of signaling proteins.

Keywords

AHL --- LuxR solos --- Quorum Sensing --- signaling --- Bacteria

Essential Pathways and Circuits of Autism Pathogenesis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199051 Year: Pages: 181 DOI: 10.3389/978-2-88919-905-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology --- Genetics
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.

Lipid Signalling In Plant Development And Responses To Environmental Stresses

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199105 Year: Pages: 112 DOI: 10.3389/978-2-88919-910-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Botany
Added to DOAB on : 2016-01-19 14:05:46
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In response to environmental stresses, or during development, plant cells will produce lipids that will act as intracellular or intercellular mediators. Glycerophospholipid and/or sphingolipid second messengers resulting from the action of lipid metabolizing enzymes (e.g. lipid-kinases or lipases) are commonly found within cells. The importance of such mediating lipids in plants has become increasingly apparent. Responses to biotic and abiotic stresses, and to plant hormones, all appear to involve and require lipid signals. Likewise, developmental processes, in particular polarized growth, seem also to involve signalling lipids. Amongst these lipids, phosphatidic acid (PA) has received the most attention. It can be produced by phospholipases D, but also by diacylglycerol kinases coupled to phospholipases C. Proteins that bind phosphatidic acid, and for which the activity is altered upon binding, have been identified. Furthermore, other lipids are also important in signalling processes. PA can be phosphorylated into diacylglycerol-pyrophosphate, and plants are one of the first biological models where the production of this lipid has been reported, and its implication in signal transduction have been demonstrated. PA can also be deacylated into lyso- phosphatidic acid. The phosphorylated phosphatidylinositols, i.e. the phosphoinositides, can act as substrate of phospholipases C, but are also mediating lipids per se, since proteins that bind them have been identified. Other important lipid mediators belong to the sphingolipid family such the phosphorylated phytosphingosine, or long-chain bases. Many questions remain unanswered concerning lipid signalling in plants. Understanding and discussing current knowledge on these mechanisms will provide insights into plant mechanisms in response to constraints, either developmental or environmental.

Homeostatic and retrograde signaling mechanisms modulating presynaptic function and plasticity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197040 Year: Pages: 152 DOI: 10.3389/978-2-88919-704-0 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Activity within neural circuits shapes the synaptic properties of component neurons in a manner that maintains stable excitatory drive, a process referred to as homeostatic plasticity. These potent and adaptive mechanisms have been demonstrated to modulate activity at the level of an individual neuron, synapse, circuit, or entire network, and dysregulation at some or all of these levels may contribute to neuropsychiatric disorders, intellectual disability, and epilepsy. Greater mechanistic understanding of homeostatic plasticity will provide key insights into the etiology of these disorders, which may result from network instability and synaptic dysfunction. Over the past 15 years, the molecular mechanisms of this form of plasticity have been intensely studied in various model organisms, including invertebrates and vertebrates. Though once thought to have a predominantly postsynaptic basis, emerging evidence suggests that homeostatic mechanisms act on both sides of the synapse through mechanisms such as retrograde signaling, to orchestrate compensatory adaptations that maintain stable network function. These trans-synaptic signaling systems ultimately alter neurotransmitter release probability by a variety of mechanisms including changes in vesicle pool size and calcium influx. These adaptations are not expected to occur homogenously at all terminals of a pre-synaptic neuron, as they might synapse with neurons in non-overlapping circuits. However, the factors that govern the homeostatic control of synapse-specific plasticity are only beginning to be understood. In addition to our limited molecular understanding of pre-synaptic homeostatic plasticity, very little is known about its prevalence in vivo or its physiological and disease relevance. In this research topic, we aim to fill the aforementioned void by covering a broad range of topics that include:- Identification of signaling pathways and mechanisms that operate globally or locally to induce specific pre-synaptic adaptations- The nature of pre-synaptic ion channels relevant to this form of plasticity and their synapse-specific modulation and trafficking- Development and utilization of new tools or methods to study homeostatic plasticity in axons and pre-synaptic terminals- Novel mechanisms of homeostatic adaptations in pre-synaptic neurons- Postsynaptic sensors of activity and retrograde synaptic signaling systems- A comprehensive analysis of the kinds of pre-synaptic adaptations in diverse neural circuits and cell types- Identification of physiological or developmental conditions that promote pre-synaptic homeostatic adaptations- How activity-dependent (Hebbian) and homeostatic synaptic changes are integrated to both permit sufficient flexibility and maintain stable activity- Relevance of pre-synaptic homeostatic plasticity to the etiology of neuropsychiatric disorders- Computational modeling of pre-synaptic homeostatic plasticity and network stability.

Enterotoxins: Microbial Proteins and Host Cell Dysregulation

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ISBN: 9783038421634 9783038421641 Year: Pages: 306 DOI: 10.3390/books978-3-03842-164-1 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Added to DOAB on : 2016-06-03 11:14:38
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Frontiers in the Pharmacological Manipulation of Intracellular cAMP Levels

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198153 Year: Pages: 191 DOI: 10.3389/978-2-88919-815-3 Language: English
Publisher: Frontiers Media SA
Subject: Therapeutics --- Science (General)
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Cyclic adenosine monophosphate (cAMP) is a second messenger of paramount biological importance, involved in the regulation of a significant number of cellular functions through the cAMP-dependent intracellular signal transduction pathways. The aim of this "Frontiers in Pharmacology" Research Topic was to attract contributions that highlight emerging ideas in the cAMP field that: (i) describe its role in cellular function and homeostasis, (ii) present the current approaches to its pharmacological manipulation, and (iii) clarify its central role in the development of more targeted therapeutic approaches toward a spectrum of diseases. The present collection of articles highlights, in a representative (but certainly not exhaustive) way, the research activity and emerging concepts in the field, while it also reveals the therapeutic potential that targeted pharmacological manipulation of intracellular cAMP levels could exert on a number of pathological conditions.

Amino Acids of the Glutamate Family: Functions beyond Primary Metabolism

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199365 Year: Pages: 206 DOI: 10.3389/978-2-88919-936-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Botany
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The life of proteins starts and ends as amino acids. In addition to the primary function as protein building blocks, amino acids serve multiple other purposes to make a plant's life worth living. This is true especially for the amino acids of the glutamate family, namely glutamate (Glu), glutamine (Gln), proline (Pro) and arginine (Arg), as well as the product of Glu decarboxylation, ?-aminobutyric acid (GABA). Synthesis, accumulation, interconversion and degradation of these five compounds contribute in many ways to the regulation of plant development and to responses to environmental challenges. Glu and Gln hold key positions as entry points and master regulators of nitrogen metabolism in plants, and have a pivotal role in the regulatory interplay between carbon and nitrogen metabolism. Pro and GABA are among the best-studied compatible osmolytes that accumulate in response to water deficit, yet the full range of protective functions is still to be revealed. Arg, with its exceptionally high nitrogen-to-carbon ratio, has long been recognized as a major storage form of organic nitrogen. Most of the enzymes involved in metabolism of the amino acids of the glutamate family in plants have been identified or can be predicted according to similarity with animal or microbial homologues. However, for some of these enzymes the detailed biochemical properties still remain to be determined in order to understand activities in vivo. Additionally, uncertainties regarding the subcellular localization of proteins and especially the lack of knowledge about intracellular transport proteins leave significant gaps in our understanding of the metabolic network connecting Glu, Gln, Pro, GABA and Arg. While anabolic reactions are distributed between the cytosol and chloroplasts, catabolism of the amino acids of the glutamate family takes place in mitochondria and has been implicated in fueling energy-demanding physiological processes such as root elongation, recovery from stress, bolting and pollen tube elongation. Exceeding the metabolic functions, the amino acids of the glutamate family were recently identified as important signaling molecules in plants. Extracellular Glu, GABA and a range of other metabolites trigger responses in plant cells that resemble the actions of Glu and GABA as neurotransmitters in animals. Plant homologues of the Glu-gated ion channels from mammals and protein kinase signaling cascades have been implicated in these responses. Pollen tube growth and guidance depend on GABA signaling and the root architecture is specifically regulated by Glu. GABA and Pro signaling or metabolism were shown to contribute to the orchestration of defense and programmed cell death in response to pathogen attacks. Pro signaling was additionally proposed to regulate developmental processes and especially sexual reproduction. Arg is tightly linked to nitric oxide (NO) production and signaling in plants, although Arg-dependent NO-synthases could still not be identified. Potentially Arg-derived polyamines constitute the missing link between Arg and NO signaling in response to stress. Taken together, the amino acids of the glutamate family emerge as important signaling molecules that orchestrate plant growth and development by integrating the metabolic status of the plant with environmental signals, especially in stressful conditions. This research topic collects contributions from different facets of glutamate family amino acid signaling or metabolism to bring together, and integrate in a comprehensive view the latest advances in our understanding of the multiple functions of Glu-derived amino acids in plants.

Golgi Pathology in Neurodegenerative Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197576 Year: Pages: 119 DOI: 10.3389/978-2-88919-757-6 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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The Golgi apparatus is a central organelle that lies at the heart of the secretory pathway. It ensures post-translational protein modifications such as glycosylation and cleavage as well as protein sorting to neuronal axons and dendrites. Structural and functional alterations of the Golgi apparatus (fragmentation and atrophy), which are collectively termed Golgi pathology, are now recognized as a constant feature of many neuro-degenerative diseases. However, the molecular mechanisms underlying these changes and their precise relevance to neurodegeneration have not yet been completely elucidated. This eBook contains 13 reviews that address the molecular mechanisms of Golgi pathology in Parkinson and Alzheimer diseases, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies, and discuss their potential relevance to the pathological loss of neuronal cell bodies, axons and synapses.

Crosstalk between the osteogenic and neurogenic stem cell niches: how far are they from each other?

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197774 Year: Pages: 102 DOI: 10.3389/978-2-88919-777-4 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Somatic stem cells reside in definite compartments, known as “niches”, within developed organs and tissues, being able to renew themselves, differentiate and ensure tissue maintenance and repair. In contrast with the original dogmatic distinction between renewing and non-renewing tissues, somatic stem cells have been found in almost every human organ, including brain and heart. The adult bone marrow, in particular, houses a complex multifunctional niche comprising hemopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs), that intensely interact. HSCs represent the common precursors of all mature blood cells. MSCs are instead able to differentiate along multiple mesodermal lineages and are believed to represent the key somatic stem cell within the skeletogenic niche, being conceptually able to produce any tissue included within a mature skeletal segment (bone, cartilage, blood vessels, adipose tissue, and supporting connective stroma). Despite this high plasticity, the claim that MSCs could be capable of transdifferentiation along non-mesodermal lineages, including neurons, has been strongly argued. Adult osteogenic and neurogenic niches display wide differences: embryo origin, microenvironment, progenitors’ lifespan, lineages of supporting cells. Although similar pathways may be involved, it is hard to believe that the osteogenic and neurogenic lineages can share functional features. The outbreaking research achievements in the field of regenerative medicine, along with the pressing need for effective innovative tools for the treatment of neurodegeneration and neurologic disorders, have been forcing experimental clinical applications, which, despite their scientific weakness, have recently stimulated the public opinion. Based on this contemporary background, this Research Topic wish to provide an in-depth revision of the state of the art on relevant scientific milestones addressing the differences and possible interconnections and overlaps, between the osteogenic and the neurogenic niches. Dissertations on both basic research and clinical aspects, along with ethical and regulatory issues on the use of somatic stem cells for in vivo transplantation, have been covered.

Mitochondrial Dysfunction in Ageing and Diseases

ISBN: 9783038422518 9783038422525 Year: Pages: XXVI, 516 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Added to DOAB on : 2016-08-16 07:37:51
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The past decade has witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into ageing and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in ageing and in several diseases, many of which are age-related, including mitochondrial diseases, cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Additionally, a possible link between mitochondrial metabolism and the ubiquitin-proteasome and autophagy-lysosome systems is emerging as a novel factor contributing to the progression of several human diseases. This special issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing in the vast field of mitochondrial biology. These include, but are not limited to: ageingneurodegenerative diseasesmitochondrial diseasesmetabolic diseasesprotein homeostasiscell/retrograde signalingoxidative stresspaincancerimmune systemtherapies to counteract mitochondrial dysfunction

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2016 (10)