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The microbial nitrogen cycle

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194124 Year: Pages: 174 DOI: 10.3389/978-2-88919-412-4 Language: English
Publisher: Frontiers Media SA
Subject: Microbiology --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Nitrogen is an essential element in biological systems, and one that often limits production in both aquatic and terrestrial systems. Due to its requirement in biological macromolecules, its acquisition and cycling have the potential to structure microbial communities, as well as to control productivity on the ecosystem scale. In addition, its versatile redox chemistry is the basis of complex biogeochemical transformations that control the inventory of fixed nitrogen, both in local environments and over geological time. Although many of the pathways in the microbial nitrogen cycle were described more than a century ago, additional fundamental pathways have been discovered only recently. These findings imply that we still have much to learn about the microbial nitrogen cycle, the organisms responsible for it, and their interactions in natural and human environments. Progress in nitrogen cycle research has been facilitated by recent rapid technological advances, especially in genomics and isotopic approaches. In this Research Topic, we reviewed the leading edge of nitrogen cycle research based on these approaches, as well as by exploring microbial processes in modern ecosystems.

Microbial Connections Between the Subsurface Sulfur Cycle and Other Elemental Cycles

Authors: --- --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889456529 Year: Pages: 213 DOI: 10.3389/978-2-88945-652-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Microbiology --- Geography
Added to DOAB on : 2019-01-23 14:53:43
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Sulfur has many redox states and is a major metabolite in suboxic and anaerobic environments including, but not restricted to, marine and marginal marine sediments, the water column of oxygen minimum zones, salt marshes and oil wells. Microbially mediated redox cycling of sulfur typically comprises dissimilatory sulfate reduction (MSR), sulfide reoxidation, disproportionation and the oxidation and reduction of sulfur redox intermediates. These processes contribute to the degradation of organic matter, link the cycles of sulfur and carbon, control the production and consumption of methane and are critical for the long term budget of O2 in the atmosphere. Microbial and abiotic processes at redox interfaces also connect the sulfur cycle to the redox cycles of nitrogen, iron and other elements, producing distinctive geochemical and molecular signatures. Studies that couple microbiology with stable isotope geochemistry have informed interpretations of microbial sulfur cycling in modern and past environments. Laboratory-based studies and models of MSR have sought to understand the physiological and environmental controls of the magnitude of sulfur isotope fractionation. The fractionations of stable sulfur and oxygen isotopes during MSR are also used to track enzymatic activity during MSR and processes that oxidize sulfide in the presence of environmental oxidants. Outstanding questions in the field concern the importance of oxidative processes within the natural environment, the delivery of oxidants and carbon sources to the zones of sulfate reduction and the ability to detect or reconstruct oxidative processes from the chemical, isotopic, metagenomic, transcriptomic, proteomic and metabolomics profiles in the environment. Recent studies have emphasized the complex connections between sulfur and methane, iron, nitrogen and other elements. These links may involve the redox cycling of species that occur at concentrations difficult to detect by standard geochemical techniques or that are cycled at very rapid rates (cryptic cycles). Of particular interest is the use of isotope geochemistry to quantify links among various electron acceptors, including sulfate, ferric iron, and nitrate, during the anaerobic methane oxidation. For example, recent geochemical measurements have hinted that microbial sulfate reduction coupled to organic matter oxidation is mechanistically different to when sulfate reduction is coupled to methane oxidation. Recent studies have also suggested a possible contribution of a number of previously uncultured microbial groups in sulfur cycling in sulfidic environments, inspiring further studies of these organisms and their partnerships in anaerobic environments. This Research Topic highlights studies of microbial interactions, processes and communities that couple the sulfur cycle to the cycles of other elements in aphotic environments.

Maintenance of Genome Integrity: DNA Damage Sensing, Signaling, Repair and Replication in Plants

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198207 Year: Pages: 129 DOI: 10.3389/978-2-88919-820-7 Language: English
Publisher: Frontiers Media SA
Subject: Botany --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Environmental stresses and metabolic by-products can severely affect the integrity of genetic information by inducing DNA damage and impairing genome stability. As a consequence, plant growth and productivity are irreversibly compromised. To overcome genotoxic injury, plants have evolved complex strategies relying on a highly efficient repair machinery that responds to sophisticated damage perception/signaling networks. The DNA damage signaling network contains several key components: DNA damage sensors, signal transducers, mediators, and effectors. Most of these components are common to other eukaryotes but some features are unique to the plant kingdom. ATM and ATR are well-conserved members of PIKK family, which amplify and transduce signals to downstream effectors. ATM primarily responds to DNA double strand breaks while ATR responds to various forms of DNA damage. The signals from the activated transducer kinases are transmitted to the downstream cell-cycle regulators, such as CHK1, CHK2, and p53 in many eukaryotes. However, plants have no homologue of CHK1, CHK2 nor p53. The finding of Arabidopsis transcription factor SOG1 that seems functionally but not structurally similar to p53 suggests that plants have developed unique cell cycle regulation mechanism. The double strand break repair, recombination repair, postreplication repair, and lesion bypass, have been investigated in several plants. The DNA double strand break, a most critical damage for organisms are repaired non-homologous end joining (NHEJ) or homologous recombination (HR) pathway. Damage on template DNA makes replication stall, which is processed by translesion synthesis (TLS) or error-free postreplication repair (PPR) pathway. Deletion of the error-prone TLS polymerase reduces mutation frequencies, suggesting PPR maintains the stalled replication fork when TLS is not available. Unveiling the regulation networks among these multiple pathways would be the next challenge to be completed. Some intriguing issues have been disclosed such as the cross-talk between DNA repair, senescence and pathogen response and the involvement of non-coding RNAs in global genome stability. Several studies have highlighted the essential contribution of chromatin remodeling in DNA repair. DNA damage sensing, signaling and repair have been investigated in relation to environmental stresses, seed quality issues, mutation breeding in both model and crop plants and all these studies strengthen the idea that components of the plant response to genotoxic stress might represent tools to improve stress tolerance and field performance. This focus issue gives researchers the opportunity to gather and interact by providing Mini-Reviews, Commentaries, Opinions, Original Research and Method articles which describe the most recent advances and future perspectives in the field of DNA damage sensing, signaling and repair in plants. A comprehensive overview of the current progresses dealing with the genotoxic stress response in plants will be provided looking at cellular and molecular level with multidisciplinary approaches. This will hopefully bring together valuable information for both plant biotechnologists and breeders.

Cell Fate

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198528 Year: Pages: 102 DOI: 10.3389/978-2-88919-852-8 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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The fundamental question of how an undifferentiated progenitor cell adopts a more specialized cell fate that then contributes to the development of specialized tissues, organs, organ systems and ultimately a unique individual of a given species has intrigued cell and developmental biologists for many years. Advances in molecular and cell biology have enabled investigators to identify genetic and epigenetic factors that contribute to these processes with increasing detail and also to define the various molecular characteristics of each cell fate with greater precision. Understanding these processes have also provided greater insights into disorders in which the normal mechanisms of cell fate determination are altered, such as in cancer and inherited malformations. With these advances have come techniques that facilitate the manipulation of cell fate, which have the potential to revolutionize the field of medicine by facilitating the repair and/or regeneration of diseased organs. Given the rapid advances that are occurring in the field, the articles in this eBook are both relevant and timely. These articles originally appeared online as part of the Research Topic “Cell Fate” overseen by my colleagues Dr. Lin, Dr. Buttitta, Dr. Maves, Dr. Dilworth, Dr. Paladini and myself and have been viewed extensively. Because of their popularity, they are now made available as an eBook, in a more easily downloadable form.Michael T. Chin

Cancer-associated defects in the DNA damage response: drivers for malignant transformation and potential therapeutic targets

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199495 Year: Pages: 107 DOI: 10.3389/978-2-88919-949-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Genetics
Added to DOAB on : 2016-01-19 14:05:46
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For this eBook, and the associated Research Topic in Frontiers in Genetics, entitled: ‘Cancer-associated defects in the DNA damage response: drivers for malignant transformation and potential therapeutic targets’ we have selected 10 papers that each discusses important, yet distinct aspects of the response to DNA damage in normal cells and cancer cells. Using an evolutionary conserved signaling network called the ‘DNA damage response (DDR)’ cells maintain the integrity of their genome, and thus safeguard cellular functioning and the ability to create viably progeny. Initially, the DDR appeared to consist of few linear kinase-driven pathways. However, research over the past decades in model organisms, as well as in the human system has revealed that the DDR is a complex signaling network, wired by multiple parallel pathways and displaying extensive crosstalk. Besides phosphorylation, multiple other post-translational modifications, including ubiquitination and sumoylation, are involved to achieve chromatin remodeling and initiation of DNA repair. Also, rather than being a cell-intrinsic phenomenon, we increasingly appreciate that cell-cell communication is involved. The recognition and repair of DNA damage is essential to maintain normal physiology. Multiple pathological conditions have been attributed to defective DNA repair, most notably accelerated aging, neurodegeneration and cancer. In the context of cancer, through repair of DNA damage or elimination of irreparably damaged cells, the DDR clearly has a tumor-suppressive role. Indeed, many tumor cells show partially inactivated DDR signaling, which allows proliferation in the context of DNA damage-inducing oncogenes. Simultaneously, loss of specific DDR signaling nodes creates a specific dependence of tumor cells on their remaining DDR components, and thus creates therapeutic opportunities. Especially in the context of cancer treatment, numerous targeted agents are under investigation, either to potentiate the cytotoxic effects of chemo-radiotherapy, or to induce synthetic lethality with cancer-specific alterations, with the treatment of BRCA1/2 mutant cancers with PARP1 inhibitors as a prototype example. We have selected four review articles that provide insight into the key components and the wiring of the DDR and DNA repair. Torgovnick and Schumacher review the involvement of DNA repair in the initiation and treatment of cancer, Brinkmann et al., describe the involvement of ubiquitination in DNA damage signaling and Jaiswal and Lindqvist discuss how cell-extrinsic signaling participates in communication of DNA damage to neighboring cells. In addition, Shatneyeva and colleagues review the connection between the cellular response to DNA damage and escape from immune surveillance. Concerning the therapeutic application of targeting the DDR and DNA repair, three articles were included. Krajewska and van Vugt review the wiring of homologous recombination and how this offers therapeutic opportunities. Additionally, Knittel and colleagues describe how genetic loss of the central DDR component ATM in chronic lymphocytic leukemia can be exploited therapeutically by targeting certain parallel DNA repair pathways. Syljuasen and colleagues report on how targeting of the DDR can be used as a therapeutic strategy in lung cancer. Finally, three chapters describe newly identified regulators of the cellular response to DNA damage. Von Morgen et al. describe the R2TP complex, Lezzi and Fanciluuli review the involvement of Che-1/AATF in the DDR, and Ohms and co-authors describe how retrotransposons are at the basis of increased genomic instability. Altogether, these articles describe how defective responses to DNA damage underlie disease - and especially in the context of cancer -can be exploited to better treat disease.

In vivo Cell Biology of Cerebral Cortical Development and Its Related Neurological Disorders: Cellular Insights into Neurogenesis and Neuronal Migration

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199624 Year: Pages: 268 DOI: 10.3389/978-2-88919-962-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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The brain consists of a complex but precisely organized neural network, which provides the structural basis of higher order functions. Such a complex structure originates from a simple pseudostratified neuroepithelium. During the developing mammalian cerebral cortex, a cohort of neural progenitors, located near the ventricle, differentiates into neurons and exhibits multi-step modes of migration toward the pial surface. Tight regulation of neurogenesis and neuronal migration is essential for the determination of the neuron number in adult brains and the proper positioning of excitatory and inhibitory neurons in a specific layer, respectively. In addition, defects in neurogenesis and neuronal migration can cause several neurological disorders, such as microcephaly, periventricular heterotopia and lissencephaly. Recent advances in genetic approaches to study the developing cerebral cortex, as well as the use of a number of novel techniques, particularly in vivo electroporation and time-lapse analyses using explant slice cultures, have significantly increased our understanding of cortical development. These novel techniques have allowed for cell biological analyses of cerebral cortical development in vivo or ex vivo, showing that many cellular events, including endocytosis, cell adhesion, microtubule and actin cytoskeletal regulation, neurotransmitter release, stress response, the consequence of cellular crowding (physical force), dynamics of transcription factors, midbody release and polarity transition are required for neurogenesis and/or neuronal migration. The aim of this research topic is to highlight molecular and cellular mechanisms underlying cerebral cortical development and its related neurological disorders from the cell biological point of views, such as cell division, cell-cycle regulation, cytoskeletal organization, cell adhesion and membrane trafficking. The topic has been organized into three chapters: 1) neurogenesis and cell fate determination, 2) neuronal migration and 3) cortical development-related neurological disorders. We hope that the results and discussions contributed by all authors in this research topic will be broadly useful for further advances in basic research, as well as improvements in the etiology and care of patients suffering from neurological and psychiatric disorders.

From Sex Differences in Neuroscience to a Neuroscience of Sex Differences: New Directions and Perspectives

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196890 Year: Pages: 199 DOI: 10.3389/978-2-88919-689-0 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Medicine (General) --- Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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This research topic aims to integrate scattered findings on sex differences in neuroscience into a broader theory of how the human brain is shaped by sex and sex hormones in order to cause the great variety of sex differences that are commonly observed. It can be assumed that these differences didn’t occur arbitrarily, but that they rather determined and still determine evolutionary success of individuals and were shaped by the processes of natural and in particular sexual selection. Therefore, sex differences are not negligible and sex difference research cannot be discriminating against one sex or the other. In fact a better understanding of the underlying causes of sex differences has great advantages for both men and women and society as a whole, not only in terms of health care, but in every aspect of life. Gender equality can only work out if it is equally well understood for men and women what their individual resources and needs are. Therefore, it is of great importance to pave the way for identifying the underlying principles of structural and functional brain organization that cause men and women to act, think and feel differently. To this end it is of particular interest to identify possible similarities and interrelations between sex differences that did so far stand separately, in order to investigate whether they share a common source. To understand, where a specific sex difference comes from and whether or not it is caused by the same principle as other sex differences, it is necessary to explicitly link sex differences in behavior to their neuronal correlates and vice versa link sex differences in brain structure and function to their behavioral outcomes. In particular a new understanding of male and female brain functioning may arise from findings on how sex hormones interact with various neurotransmitter systems. In the past few years several findings demonstrated that women’s behavior is influenced by the sex hormone fluctuations they experience naturally during their menstrual cycle to the extent that sex differences may only be detectable in one cycle phase but not another. The study of menstrual cycle dependent effects gives important hints about which sex differences are activational and which are organizational. Additionally it only recently came to attention, that hormonal contraception may alter a women’s mood, cognition and behavior as a consequence of changes in brain structure and function. The underlying mechanisms are so poorly understood that it is even hard to predict, whether hormonal contraception will mask or amplify sex differences in a given task. Since the oral hormonal contraceptive pill is meanwhile used by 100 million women worldwide and even by teenagers whose brains are not yet fully developed, the question of how the synthetic steroids contained in hormonal contraceptives act on the brain is to be studied hand in hand with naturally occurring sex differences. This topic summarizes the current state of the art in sex difference research and gives new perspectives in terms of hypothesis generation an methodology. Both are necessary to gain a complete picture of what it is that makes a brain male or female and move towards a neuroscience of sex differences.

Transcriptional Regulation in Cancers and Metabolic Diseases

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197125 Year: Pages: 98 DOI: 10.3389/978-2-88919-712-5 Language: English
Publisher: Frontiers Media SA
Subject: Oncology --- Medicine (General) --- Internal medicine
Added to DOAB on : 2016-04-07 11:22:02
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The transcription factor (TF) mediated regulation of gene expression is a process fundamental to all biological and physiological processes. Genetic changes and epigenetic modifications of TFs affect target gene expression during the formation of malignant cells. Extensive work has been done on the critical TFs in various disease models. Despite the success of numerous TF-targeted therapies, there remain significant hurdles understanding the mechanisms, transcriptional targets and networks of physiologic pathways that govern TF action. This effort is now beginning to produce exciting new avenues of research. A clinically relevant topic for genetic change of TF is the mutant isoforms of p53, the most famous tumor suppressor. The p53 mutations either results in loss of function, or acting as dominant negative for wild-type protein, or ‘gain of function’ specifically promoting cancer survival. The gain of function is achieved by shifting p53 binding partner proteins, or changed genomic binding landscape leading to a cancer-promoting transcriptome. Another example of genetic change of TF causing malignancy is the AML-ETO fusion protein in the human t(8;21)-leukemia. The fusion protein is an active TF, and more interestingly, new studies link the disease causing role of AML-ETO to the unique transcriptome in the hematopoietic stem cells. Nuclear receptors (NR) are a group of ligand-dependent TFs governing the expression of genes involved in a broad range of reproductive, developmental and metabolic programs. Genetic changes and epigenetic modifications of NRs lead to cancers and metabolic diseases. Androgen receptor (AR), estrogen receptor (ER) and progesterone receptor (PR) are well studied NRs in prostate, breast and endometrial cancers. The development in sequencing technology and computational genomics enable us to investigate the transcription programs of these master TFs in an unprecedented level. This Research Topic aims to present the most up-to-date progress in the field of transcription regulation in cancers and metabolic diseases.

The Origin of the Plasma Cell Heterogeneity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197347 Year: Pages: 80 DOI: 10.3389/978-2-88919-734-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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Plasma cells (PCs) are terminally differentiated B-cells producing large amounts of immunoglobulins (Ig). In humans, most of circulating Ig are produced by bone marrow plasma cells. PCs differentiate from activated naïve or memory B-cells usually activated by specific antigens. It is still controversial whether the regulation of PCs numbers and the “active” in vivo Ig diversity depend or not on non-specific reactivation of B-cells during infections. Depending on the stimulus (T-independent/T-dependent antigen, cytokines, partner cells) and B-cell types (naïve or memory, circulating or germinal center, lymph nodes or spleen, B1 or B2...), both the phenotype and isotype of PCs differ suggesting that PC diversity is either linked to B-cell diversity or to the type of stimulus or to both. Knowledge of the mechanisms supporting PC diversity has important consequences for the management of i) plasma cell neoplasia such as Multiple Myeloma and Waldenström's Macroglobulinemia, ii) vaccine protection against pathogens and iii) auto-immune diseases.

Keywords

Plasma cell --- B-cell --- differentiation --- Cell Cycle --- IL21 --- Autophagy --- B1 --- Autoimmunity --- Myeloma

The metabolic challenges of immune cells in health and disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196227 Year: Pages: 80 DOI: 10.3389/978-2-88919-622-7 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-08-16 10:34:25
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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.

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