scholarly journals Autophagic Machinery of Plant Peroxisomes

2019 ◽  
Vol 20 (19) ◽  
pp. 4754 ◽  
Author(s):  
Sławomir Borek ◽  
Szymon Stefaniak ◽  
Jan Śliwiński ◽  
Małgorzata Garnczarska ◽  
Małgorzata Pietrowska-Borek
Keyword(s):  
Molecular Mechanisms ◽  
Glyoxylate Cycle ◽  
Plant Cells ◽  
Physiological Role ◽  
Signal Molecules ◽  
Cell Organelles ◽  
Selective Degradation ◽  
Leaf Peroxisomes ◽  
The Glyoxylate Cycle

Peroxisomes are cell organelles that play an important role in plants in many physiological and developmental processes. The plant peroxisomes harbor enzymes of the β-oxidation of fatty acids and the glyoxylate cycle; photorespiration; detoxification of reactive oxygen and nitrogen species; as well as biosynthesis of hormones and signal molecules. The function of peroxisomes in plant cells changes during plant growth and development. They are transformed from organelles involved in storage lipid breakdown during seed germination and seedling growth into leaf peroxisomes involved in photorespiration in green parts of the plant. Additionally, intensive oxidative metabolism of peroxisomes causes damage to their components. Therefore, unnecessary or damaged peroxisomes are degraded by selective autophagy, called pexophagy. This is an important element of the quality control system of peroxisomes in plant cells. Despite the fact that the mechanism of pexophagy has already been described for yeasts and mammals, the molecular mechanisms by which plant cells recognize peroxisomes that will be degraded via pexophagy still remain unclear. It seems that a plant-specific mechanism exists for the selective degradation of peroxisomes. In this review, we describe the physiological role of pexophagy in plant cells and the current hypotheses concerning the mechanism of plant pexophagy.

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

2018 ◽  
Vol 25 (1) ◽  
pp. 5-21 ◽  
Author(s):  
Ylenia Cau ◽  
Daniela Valensin ◽  
Mattia Mori ◽  
Sara Draghi ◽  
Maurizio Botta
Keyword(s):  
Protein Interactions ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
Specific Protein ◽  
Protein Protein Interactions ◽  
Cellular Processes ◽  
Protein Partners ◽  
High Sequence Homology ◽  
Small Molecule Modulators

14-3-3 is a class of proteins able to interact with a multitude of targets by establishing protein-protein interactions (PPIs). They are usually found in all eukaryotes with a conserved secondary structure and high sequence homology among species. 14-3-3 proteins are involved in many physiological and pathological cellular processes either by triggering or interfering with the activity of specific protein partners. In the last years, the scientific community has collected many evidences on the role played by seven human 14-3-3 isoforms in cancer or neurodegenerative diseases. Indeed, these proteins regulate the molecular mechanisms associated to these diseases by interacting with (i) oncogenic and (ii) pro-apoptotic proteins and (iii) with proteins involved in Parkinson and Alzheimer diseases. The discovery of small molecule modulators of 14-3-3 PPIs could facilitate complete understanding of the physiological role of these proteins, and might offer valuable therapeutic approaches for these critical pathological states.

The role of the glyoxylate cycle in the symbiotic fungus Tuber borchii: expression analysis and subcellular localization

2007 ◽  
Vol 52 (3-4) ◽  
pp. 159-170 ◽  
Author(s):  
Simona Abba’ ◽  
Raffaella Balestrini ◽  
Alessandra Benedetto ◽  
Hanspeter Rottensteiner ◽  
José Ramón De Lucas ◽  
...  
Keyword(s):  
Subcellular Localization ◽  
Expression Analysis ◽  
Glyoxylate Cycle ◽  
Tuber Borchii ◽  
Symbiotic Fungus ◽  
The Glyoxylate Cycle

Essential Roles for Mef2c in Lymphoid Commitment and B-Cell Function.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 377-377
Author(s):  
Sandra Stehling-Sun ◽  
Rebecca Jimenez ◽  
Andrew Hu ◽  
Fernando D. Camargo
Keyword(s):  
B Cells ◽  
B Cell ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
Cell Function ◽  
Physiological Role ◽  
Erythroid Differentiation ◽  
Hematopoietic Stem ◽  
Interleukin 7

Abstract MEF2 transcription factors are well-established regulators of muscle development. Recently, work in murine models has identified one of these factors, Mef2c, as an important regulator in the pathogenesis and the development of acute myeloid leukemia (AML). However, little is know about the molecular mechanism and physiological role of Mef2c in hematopoiesis. Using conditional gene ablation, we have discovered an unexpected role for MEF2c in hematopoietic stem cells (HSCs), where it is required for pan-lymphoid commitment. Competitive repopulation experiments using Mef2c-null HSCs deleted by means of the Mx1-Cre/poly(IC) approach, revealed completely normal monocytic, granulocytic and erythroid differentiation capacities by mutant cells. Generation and renewal of myeloid progenitors and HSCs was also normal. However, contribution to lymphoid lineages (T-cells, B-cells and natural killer cells) was dramatically reduced. Mef2c-deleted HSCs were able to generate lymphoid primed multipotent progenitors (LMPPs) and expressed normal levels of Flt-3 and the master lymphoid regulator ikaros. However, expression of the interleukin-7 receptor (IL-7R) and the number of phenotypically defined common lymphoid progenitors (CLPs) were substantially reduced. We have found two conserved Mef2c-binding sites in the promoter of the Il-7R gene, indicating that Mef2c could directly regulate Il-7R transcription. This and other potential molecular mechanisms of Mef2c-mediated lymphoid commitment will be discussed. We have also studied the effects of lineage-specific deletion of Mef2c in both myeloid and lymphoid populations. Whereas deletion in myelomonocytic cells using the LysM-Cre strain resulted in no anomalies, B-cell specific ablation with the CD19-Cre line revealed major phenotypical and functional abnormalities. CD19-Cre:Mef2cf/f mice show impaired germinal center formation and reduced antibody production in response to T-cell dependent antigens. In addition Mef2c-null mature B-cells fail to express the mature marker CD23, the low affinity receptor for IgE, which we show is a direct transcriptional target. As a consequence of CD23 reduction, CD19-Cre:Mef2cf/f mice have increased IgE production, thus indicating a potential role of Mef2c in allergic disease. Our work here sheds new light on the molecular mechanisms of lymphopoiesis and identifies MEF2 factors as critical hematopoietic transcriptional regulators.

scholarly journals miR-21 blocks obesity in mice: a potential therapy for humans

2020 ◽  
Author(s):  
Said Lhamyani ◽  
Adriana-Mariel Gentile ◽  
Rosa M. Giráldez-Pérez ◽  
Mónica Feijóo-Cuaresma ◽  
Silvana Yanina Romero-Zerbo ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Drug Targets ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Caloric Intake ◽  
Physiological Role ◽  
Expression Of Genes ◽  
Obesity In Mice ◽  
Metabolically Healthy

AbstractmicroRNAs are promising drug targets in obesity and metabolic disorders. miR-21 expression is upregulated in obese white adipose tissue (WAT); however, its physiological role in WAT has not been fully explored. We aimed to dissect the underlying molecular mechanisms of miR-21 in treating obesity, diabetes, and insulin resistance. We demonstrated, in human and mice, that elevated miR-21 expression is associated with metabolically healthy obesity. miR-21 mimic affected the expression of genes associated with adipogenesis, thermogenesis, and browning in 3T3-L1 adipocytes. In addition, it blocked high fat diet-induced weight gain in obese mice, without modifying food intake or physical activity. This was associated with metabolic enhancements, WAT browning and thermogenic programming, and brown AT induction through VEGF-A, p53, and TGFβ1 signaling pathways. Our findings add a novel role of miR-21 in the regulation of obesity and a potential therapy for both obesity and T2D without altering caloric intake and physical activities.

scholarly journals RIPK1-Associated Inborn Errors of Innate Immunity

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiahui Zhang ◽  
Taijie Jin ◽  
Ivona Aksentijevich ◽  
Qing Zhou
Keyword(s):  
Immune Deficiency ◽  
Molecular Mechanisms ◽  
Clinical Manifestations ◽  
Physiological Role ◽  
Model Organisms ◽  
Loss Of Function ◽  
Inborn Errors ◽  
Post Translational Modifications ◽  
Cell Death Signaling

RIPK1 (receptor-interacting serine/threonine-protein kinase 1) is a key molecule for mediating apoptosis, necroptosis, and inflammatory pathways downstream of death receptors (DRs) and pattern recognition receptors (PRRs). RIPK1 functions are regulated by multiple post-translational modifications (PTMs), including ubiquitination, phosphorylation, and the caspase-8-mediated cleavage. Dysregulation of these modifications leads to an immune deficiency or a hyperinflammatory disease in humans. Over the last decades, numerous studies on the RIPK1 function in model organisms have provided insights into the molecular mechanisms of RIPK1 role in the maintenance of immune homeostasis. However, the physiological role of RIPK1 in the regulation of cell survival and cell death signaling in humans remained elusive. Recently, RIPK1 loss-of-function (LoF) mutations and cleavage-deficient mutations have been identified in humans. This review discusses the molecular pathogenesis of RIPK1-deficiency and cleavage-resistant RIPK1 induced autoinflammatory (CRIA) disorders and summarizes the clinical manifestations of respective diseases to help with the identification of new patients.

Comparative analysis of Botrytis cinerea in response to the microbial secondary metabolite benzothiazole using iTRAQ-based quantitative proteomics

2020 ◽  
Author(s):  
Kaidi Cui ◽  
Leiming He ◽  
Yunhe Zhao ◽  
Wei Mu ◽  
Jin Lin ◽  
...  
Keyword(s):  
Antifungal Activity ◽  
Botrytis Cinerea ◽  
Mitochondrial Membrane ◽  
Molecular Mechanisms ◽  
Glyoxylate Cycle ◽  
Pathogenic Fungi ◽  
Phytopathogenic Fungus ◽  
Future Research ◽  
Design And Synthesis ◽  
The Glyoxylate Cycle

Benzothiazole is a microbial volatile compound with strong antifungal activity against the phytopathogenic fungus Botrytis cinerea, but its mode of action against fungi remains largely unknown. Understanding the molecular mechanisms underlying its activity could aid the design and synthesis of new similar compounds against pathogenic fungi. Based on the results of morphological and antifungal activity assays, B. cinerea was exposed to 2.5 μL/L benzothiazole for 12, 24 and 48 h, and an iTRAQ-based quantitative proteomic analysis showed that 378 out of 5,110 identified proteins were differentially expressed proteins (DEPs). The majority of these DEPs were associated with carbohydrate metabolism, oxidation-reduction processes and energy production. Further analysis showed that benzothiazole inhibited mitochondrial membrane organization and decreased the mitochondrial membrane potential of B. cinerea. In addition, the key enzymes of the glyoxylate cycle were downregulated after benzothiazole treatment, and a biochemical analysis indicated that the inhibition of the glyoxylate cycle by benzothiazole blocked nutrient availability and interfered with ATP generation. This study provides markers for future research of the molecular responses of B. cinerea to benzothiazole stress.

scholarly journals Insight into Salivary Gland Aquaporins

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1547 ◽  
Author(s):  
Claudia D’Agostino ◽  
Osama A. Elkashty ◽  
Clara Chivasso ◽  
Jason Perret ◽  
Simon D. Tran ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Physiological Role ◽  
Main Role ◽  
Osmotic Gradient ◽  
Therapeutic Approaches ◽  
Potential Therapeutic Target ◽  
Transmembrane Channel ◽  
Saliva Secretion ◽  
Insight Into

The main role of salivary glands (SG) is the production and secretion of saliva, in which aquaporins (AQPs) play a key role by ensuring water flow. The AQPs are transmembrane channel proteins permeable to water to allow water transport across cell membranes according to osmotic gradient. This review gives an insight into SG AQPs. Indeed, it gives a summary of the expression and localization of AQPs in adult human, rat and mouse SG, as well as of their physiological role in SG function. Furthermore, the review provides a comprehensive view of the involvement of AQPs in pathological conditions affecting SG, including Sjögren’s syndrome, diabetes, agedness, head and neck cancer radiotherapy and SG cancer. These conditions are characterized by salivary hypofunction resulting in xerostomia. A specific focus is given on current and future therapeutic strategies aiming at AQPs to treat xerostomia. A deeper understanding of the AQPs involvement in molecular mechanisms of saliva secretion and diseases offered new avenues for therapeutic approaches, including drugs, gene therapy and tissue engineering. As such, AQP5 represents a potential therapeutic target in different strategies for the treatment of xerostomia.

scholarly journals Mitophagy in Yeast: Molecular Mechanism and Regulation

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3569
Author(s):  
Aleksei Innokentev ◽  
Tomotake Kanki
Keyword(s):  
Molecular Mechanism ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Outer Membrane Proteins ◽  
Physiological Role ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Homeostasis ◽  
Mitochondrial Ros ◽  
Cellular Components

Mitophagy is a type of autophagy that selectively degrades mitochondria. Mitochondria, known as the “powerhouse of the cell”, supply the majority of the energy required by cells. During energy production, mitochondria produce reactive oxygen species (ROS) as byproducts. The ROS damages mitochondria, and the damaged mitochondria further produce mitochondrial ROS. The increased mitochondrial ROS damages cellular components, including mitochondria themselves, and leads to diverse pathologies. Accordingly, it is crucial to eliminate excessive or damaged mitochondria to maintain mitochondrial homeostasis, in which mitophagy is believed to play a major role. Recently, the molecular mechanism and physiological role of mitophagy have been vigorously studied in yeast and mammalian cells. In yeast, Atg32 and Atg43, mitochondrial outer membrane proteins, were identified as mitophagy receptors in budding yeast and fission yeast, respectively. Here we summarize the molecular mechanisms of mitophagy in yeast, as revealed by the analysis of Atg32 and Atg43, and review recent progress in our understanding of mitophagy induction and regulation in yeast.

scholarly journals 6S RNA Function Enhances Long-Term Cell Survival

2004 ◽  
Vol 186 (15) ◽  
pp. 4978-4985 ◽  
Author(s):  
Amy E. Trotochaud ◽  
Karen M. Wassarman
Keyword(s):  
Stationary Phase ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
Rna Regulation ◽  
Competitive Fitness ◽  
Growth Defects ◽  
6S Rna ◽  
Rna Inhibition

ABSTRACT 6S RNA was identified in Escherichia coli >30 years ago, but the physiological role of this RNA has remained elusive. Here, we demonstrate that 6S RNA-deficient cells are at a disadvantage for survival in stationary phase, a time when 6S RNA regulates transcription. Growth defects were most apparent as a decrease in the competitive fitness of cells lacking 6S RNA. To decipher the molecular mechanisms underlying the growth defects, we have expanded studies of 6S RNA effects on transcription. 6S RNA inhibition of σ70-dependent transcription was not ubiquitous, in spite of the fact that the vast majority of σ70-RNA polymerase is bound by 6S RNA during stationary phase. The σ70-dependent promoters inhibited by 6S RNA contain an extended −10 promoter element, suggesting that this feature may define a class of 6S RNA-regulated genes. We also discovered a secondary effect of 6S RNA in the activation of σS-dependent transcription at several promoters. We conclude that 6S RNA regulation of both σ70 and σS activities contributes to increased cell persistence during nutrient deprivation.

scholarly journals The Molecular Mechanisms and Physiological Role of Mitophagy in Yeast

2016 ◽  
Vol 54 (4) ◽  
pp. 266-272
Author(s):  
Kentaro FURUKAWA ◽  
Tomotake KANKI
Keyword(s):  
Molecular Mechanisms ◽  
Physiological Role
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