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From soil to seed: micronutrient movement into and within the plant

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193516 Year: Pages: 193 DOI: 10.3389/978-2-88919-351-6 Language: English
Publisher: Frontiers Media SA
Subject: Nutrition and Food Sciences --- Medicine (General) --- Botany --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Abstract

In all living organisms, essential micronutrients are cofactors of many ubiquitous proteins that participate in crucial metabolic pathways, but can also be toxic when present in excessive concentrations. In order to achieve correct homeostasis, plants need to control uptake of metals from the environment, their distribution to organs and tissues, and their subcellular compartmentalization. They also have to avoid deleterious accumulation of metals and metalloids such as Cd, As and Al. These multiple steps are controlled by their transport across various membrane structures and their storage in different organelles. Thus, integration of these transport systems required for micronutrient trafficking within the plant is necessary for physiological processes to work efficiently. To cope with the variable availability of micronutrients, plants have evolved an intricate collection of physiological and developmental processes, which are under tight control of short- and long-range signaling pathways. Understanding how plants perceive and deal with different micronutrient concentrations, from regulation to active transport, is important to completing the puzzle of plant metal homeostasis. This is an essential area of research, with several implications for plant biology, agriculture and human nutrition. There is a rising interest in developing plants that efficiently mobilize specific metals and prosper in soils with limited micronutrient availability, as well as those that can selectively accumulate beneficial micronutrients in the edible parts while avoiding contaminants such as Cd and As. However, there is still an important gap in our understanding of how nutrients reach the seeds and the relative contribution of each step in the long pathway from the rhizosphere to the seed. Possible rate-limiting steps for micronutrient accumulation in grains should be the primary targets of biotechnological interventions aiming at biofortification. Over the last 10 years, many micronutrient uptake- and transport-related processes have been identified at the molecular and physiological level. The systematic search for mutants and transcriptional responses has allowed analysis of micronutrient-signaling pathways at the cellular level, whereas physiological approaches have been particularly useful in describing micronutrient-signaling processes at the organ and whole-plant level. Large-scale elemental profiling using high-throughput analytical methodologies and their integration with both bioinformatics and genetic tools, along with metal speciation, have been used to decipher the functions of genes that control micronutrients homeostasis. In this research topic, we will follow the pathway of metal movement from the soil to the seed and describe the suggested roles of identified gene products in an effort to understand how plants acquire micronutrients from the soil, how they partition among different tissues and subcellular organelles, and how they regulate their deficiency and overload responses. We also highlight the current work on heavy metals and metalloids uptake and accumulation, the studies on metal selectivity in transporters and the cross-talk between micro and macronutrients. Thus, we believe a continued dialogue and sharing of ideas amongst plant scientists is critical to a better understanding of metal movement into and within the plant.

Ubiquitin and Ubiquitin-Relative SUMO in DNA Damage Response

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454419 Year: Pages: 183 DOI: 10.3389/978-2-88945-441-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Genetics
Added to DOAB on : 2018-11-16 17:17:57
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DNA damage response (DDR) is a term that includes a variety of highly sophisticated mechanisms that cells have evolved in safeguarding the genome from the deleterious consequences of DNA damage. It is estimated that every single cell receives tens of thousands of DNA lesions per day. Failure of DDR to properly respond to DNA damage leads to stem cell dysfunction, accelerated ageing, various degenerative diseases or cancer. The sole function of DDR is to recognize diverse DNA lesions, signal their presence, activate cell cycle arrest and finally recruit specific DNA repair proteins to fix the DNA damage and thus prevent genomic instability. DDR is composed of hundreds of spatiotemporally regulated and interconnected proteins, which are able to promptly respond to various DNA lesions. So it is not surprising that mutations in genes encoding various DDR proteins cause embryonic lethality, malignancies, neurodegenerative diseases and premature ageing. The importance of DDR for cell survival and genome stability is unquestionable, but how the sophisticated network of hundreds of different DDR proteins is spatiotemporally coordinated is far from being understood. In the last ten years ubiquitin (ubiquitination) and the ubiquitin-relative SUMO (sumoylation) have emerged as essential posttranslational modifications that regulate DDR. Beside a plethora of ubiqutin and sumo E1-activating enzymes, E2-conjugating enzymes, E3-ligases and ubiquitin/sumo proteases involved in ubiquitination and sumoylation, the complexity of ubiqutin and sumo systems is additionally increased by the fact that both ubiquitin and sumo can form a variety of different chains on substrates which govern the substrate fate, such as its interaction with other proteins, changing its enzymatic activity or promoting substrate degradation. The importance of ubiquitin/SUMO systems in the orchestration of DDR is best illustrated in patients with mutations in E3-ubiquitin ligases BRCA1 or RNF168. BRCA1 is essential for proper function of DDR and its mutations lead to triple-negative breast and ovarian cancers. RNF168 is an E3 ubiquitin ligase, which creates the ubiquitin docking platform for recruitment of different DNA damage signalling and repair proteins at sites of DNA lesion, and its mutations cause RIDDLE syndrome characterized by radiosensitivity, immunodeficiency and learning disability. In addition, recently discovered the ubiquitin receptor protein SPRTN is part of the DNA replication machinery and its mutations cause early-onset hepatocellular carcinoma and premature ageing in humans. Despite more than 700 different enzymes directly involved in ubiquitination and sumoylation processes only few of them are known to play a role in DDR. Therefore, we feel that the role of ubiquitin and the ubiquitin-related SUMO in DDR is far from being understood, and that this is the emerging field that will hugely expand in the next decade due to the rapid development of a new generation of technologies, which will allow us a more robust and precise analyses of human genome, transcriptome and proteome. In this Research Topic we provide a comprehensive overview of our current understanding of ubiquitin and SUMO pathways in all aspects of DDR, from DNA replication to different DNA repair pathways, and demonstrate how alterations in these pathways cause genomic instability that is linked to degenerative diseases, cancer and pathological ageing.

Manipulation of the cellular microbicidal response and endocytic dynamic by pathogens membrane factors

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196098 Year: Pages: 81 DOI: 10.3389/978-2-88919-609-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Internal medicine
Added to DOAB on : 2016-08-16 10:34:25
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Intracellular pathogens, such as bacteria and parasites, have evolved specialized mechanisms to survive and replicate in their host, leading to disorders and diseases. The principle of these mechanisms is to reprogram the microbicidal cell function in order to disable the host cells defence that aims to control and eliminate foreign invaders. Devoid of their defence, cells become permissive to pathogens invasion. The aim of this Research Topic is to highlight and cover recent understanding of mechanisms and molecules used by pathogens to interfere with the microbicidal function of cells. This Research Topic will focus on the reprogramming of the cellular dynamics, the immune response, the phagolysosome biogenesis and the signal transduction pathways bypathogens. Special attention will be made on non-proteic virulence factors, however this Research Topic is not restricted to non-proteic virulence factors.

Dual Specificity Phosphatases: From Molecular Mechanisms to Biological Function

Authors: ---
ISBN: 9783039216888 / 9783039216895 Year: Pages: 240 DOI: 10.3390/books978-3-03921-689-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 11:49:16
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Dual specificity phosphatases (DUSPs) constitute a heterogeneous group of protein tyrosine phosphatases with the ability to dephosphorylate Ser/Thr and Tyr residues from proteins, as well as from other non-proteinaceous substrates including signaling lipids. DUSPs include, among others, MAP kinase (MAPK) phosphatases (MKPs) and small-size atypical DUSPs. MKPs are enzymes specialized in regulating the activity and subcellular location of MAPKs, whereas the function of small-size atypical DUSPs seems to be more diverse. DUSPs have emerged as key players in the regulation of cell growth, differentiation, stress response, and apoptosis. DUSPs regulate essential physiological processes, including immunity, neurobiology and metabolic homeostasis, and have been implicated in tumorigenesis, pathological inflammation and metabolic disorders. Accordingly, alterations in the expression or function of MKPs and small-size atypical DUSPs have consequences essential to human disease, making these enzymes potential biological markers and therapeutic targets. This Special Issue covers recent advances in the molecular mechanisms and biological functions of MKPs and small-size atypical DUSPs, and their relevance in human disease.

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