Vacuolar convolution: possible mechanisms and role of phosphatidylinositol 3,5-bisphosphate

2017 ◽  
Vol 44 (8) ◽  
pp. 751 ◽  
Author(s):  
Vadim Pérez Koldenkova ◽  
Noriyuki Hatsugai
Keyword(s):  
Morphological Changes ◽  
Stomatal Closure ◽  
Plant Cells ◽  
Reversible Transformation ◽  
Large Central Vacuole ◽  
Cellular Integrity ◽  
Lytic Vacuole ◽  
Cellular Cytoskeleton

The central or lytic vacuole is the largest intracellular organelle in plant cells, but we know unacceptably little about the mechanisms regulating its function in vivo. The underlying reasons are related to difficulties in accessing this organelle without disrupting the cellular integrity and to the dynamic morphology of the vacuole, which lacks a defined structure. Among such morphological changes, vacuolar convolution is probably the most commonly observed event, reflected in the (reversible) transformation of a large central vacuole into a structure consisting of interconnected bubbles of a smaller size. Such behaviour is observed in plant cells subjected to hyperosmotic stress but also takes place in physiological conditions (e.g. during stomatal closure). Although vacuolar convolution is a relatively common phenomenon in plants, studies aimed at elucidating its execution mechanisms are rather scarce. In the present review, we analyse the available evidence on the participation of the cellular cytoskeleton and ion transporters in vacuolar morphology dynamics, putting special emphasis on the available evidence of the role played by phosphatidylinositol 3,5-bisphosphate in this process.

scholarly journals Rapid Magneto-Sonoporation of Adipose-Derived Cells

Materials ◽  
2021 ◽  
Vol 14 (17) ◽  
pp. 4877
Author(s):  
Miriam Filippi ◽  
Boris Dasen ◽  
Arnaud Scherberich
Keyword(s):  
Stem Cells ◽  
Tissue Repair ◽  
Morphological Changes ◽  
Adipose Derived Stem Cells ◽  
Resonance Imaging ◽  
Membrane Resealing ◽  
First Time ◽  
Stimulation Of

By permeabilizing the cell membrane with ultrasound and facilitating the uptake of iron oxide nanoparticles, the magneto-sonoporation (MSP) technique can be used to instantaneously label transplantable cells (like stem cells) to be visualized via magnetic resonance imaging in vivo. However, the effects of MSP on cells are still largely unexplored. Here, we applied MSP to the widely applicable adipose-derived stem cells (ASCs) for the first time and investigated its effects on the biology of those cells. Upon optimization, MSP allowed us to achieve a consistent nanoparticle uptake (in the range of 10 pg/cell) and a complete membrane resealing in few minutes. Surprisingly, this treatment altered the metabolic activity of cells and induced their differentiation towards an osteoblastic profile, as demonstrated by an increased expression of osteogenic genes and morphological changes. Histological evidence of osteogenic tissue development was collected also in 3D hydrogel constructs. These results point to a novel role of MSP in remote biophysical stimulation of cells with focus application in bone tissue repair.

Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis

2020 ◽  
Author(s):  
Yajie Li ◽  
Xinliu Zeng ◽  
Dingheng Lu ◽  
Minuo Yin ◽  
Meirong Shan ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Lipid Peroxidation ◽  
Cell Viability ◽  
Stromal Cells ◽  
Morphological Changes ◽  
Iron Accumulation ◽  
Blue Staining ◽  
Endometrial Stromal Cells

Abstract STUDY QUESTION Could erastin activate ferroptosis to regress endometriotic lesions? SUMMARY ANSWER Erastin could induce ferroptosis to regress endometriotic lesions in endometriosis. WHAT IS KNOWN ALREADY Ectopic endometrial stromal cells (EESCs) are in an iron overloading microenvironment and tend to be more sensitive to oxidative damage. The feature of erastin-induced ferroptosis is iron-dependent accumulation of lethal lipid reactive oxygen species (ROS). STUDY DESIGN, SIZE, DURATION Eleven patients without endometriosis and 21 patients with endometriosis were recruited in this study. Primary normal and ectopic endometrial stromal cells were isolated, cultured and subjected to various treatments. The in vivo study involved 10 C57BL/6 female mice to establish the model of endometriosis. PARTICIPANTS/MATERIALS, SETTING, METHODS The markers of ferroptosis were assessed by cell viability, lipid peroxidation level and morphological changes. The cell viability was measured by colorimetric method, lipid peroxidation levels were measured by flow cytometry, and morphological changes were observed by transmission electron microscopy. Immunohistochemistry and western blot were used to detect ferroportin (FPN) expression. Prussian blue staining and immunofluorescent microscopy of catalytic ferrous iron were semi-quantified the levels of iron. Adenovirus-mediated overexpression and siRNA-mediated knockdown were used to investigate the role of FPN on erastin-induced ferroptosis in EESCs. MAIN RESULTS AND THE ROLE OF CHANCE EESCs were more susceptible to erastin treatment, compared to normal endometrial stromal cells (NESCs) (P<0.05). Treatment of cultured EESCs with erastin dramatically increased the total ROS level (P<0.05, versus control), lipid ROS level (P<0.05, versus NESCs) and intracellular iron level (P<0.05, versus NESCs). The cytotoxicity of erastin could be attenuated by iron chelator, deferoxamine (DFO), and ferroptosis inhibitors, ferrostatin-1 and liproxstatin-1, (P<0.05, versus erastin) in EESCs. In EESCs with erastin treatment, shorter and condensed mitochondria were observed by electron microscopy. These findings together suggest that erastin is capable to induce EESC death by ferroptosis. However, the influence of erastin on NESCs was slight. The process of erastin-induced ferroptosis in EESCs accompanied iron accumulation and decreased FPN expression. The overexpression of FPN ablated erastin-induced ferroptosis in EESCs. In addition, knockdown of FPN accelerated erastin-induced ferroptosis in EESCs. In a mouse model of endometriosis, we found ectopic lesions were regressed after erastin administration. LARGE SCALE DATA N/A LIMITATIONS, REASONS FOR CAUTION This study was mainly conducted in primary human endometrial stromal cells. Therefore, the function of FPN in vivo need to be further investigated. WIDER IMPLICATIONS OF THE FINDINGS Our findings reveal that erastin may serve as a potential therapeutic treatment for endometriosis. STUDY FUNDING/COMPETING INTEREST(S) This research did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors. The authors declare no conflict of interest.

scholarly journals Proteasome activity is required for the stage-specific transformation of a protozoan parasite.

1996 ◽  
Vol 184 (5) ◽  
pp. 1909-1918 ◽  
Author(s):  
J González ◽  
F J Ramalho-Pinto ◽  
U Frevert ◽  
J Ghiso ◽  
S Tomlinson ◽  
...  
Keyword(s):  
Essential Role ◽  
Morphological Changes ◽  
Protozoan Parasite ◽  
Eukaryotic Cells ◽  
Cysteine Proteinases ◽  
Axenic Medium ◽  
Cytoplasmic Proteins ◽  
Intracellular Parasites

A prominent feature of the life cycle of intracellular parasites is the profound morphological changes they undergo during development in the vertebrate and invertebrate hosts. In eukaryotic cells, most cytoplasmic proteins are degraded in proteasomes. Here, we show that the transformation in axenic medium of trypomastigotes of Trypanosoma cruzi into amastigote-like organisms, and the intracellular development of the parasite from amastigotes into trypomastigotes, are prevented by lactacystin, or by a peptide aldehyde that inhibits proteasome function. Clasto-lactacystin, an inactive analogue of lactacystin, and cell-permeant peptide aldehyde inhibitors of T. cruzi cysteine proteinases have no effect. We have also identified the 20S proteasomes from T. cruzi as a target of lactacystin in vivo. Our results document the essential role of proteasomes in the stage-specific transformation of a protozoan.

Role of Pyrophosphate: Fructose-6-phosphate 1-Phosphotransferase in Glycolysis in Cultured Catharanthus roseus Cells

1987 ◽  
Vol 42 (11-12) ◽  
pp. 1215-1222 ◽  
Author(s):  
Hiroshi Ashihara ◽  
Tiharu Horikosi
Keyword(s):  
Catalytic Activity ◽  
Carbohydrate Metabolism ◽  
Catharanthus Roseus ◽  
Plant Cells ◽  
Sodium Pyrophosphate ◽  
Fresh Weight

The maximum catalytic activity of pyrophosphate: fructosc-6-phosphate 1-phosphotransferase (PPi-PFK) was approximately three fold greater than that of ATP: fructosc-6-phosphate 1-phosphotransferase (ATP-PFK) in Catharanthus roseus cells at any stage of culture. The levels of both enzymes increased after subculture of the cells, reached their maximum levels on day 3-4, and then decreased. PPi-PFK partially purified from Catharanthus roseus required fructose-2,6-bis- phosphate (F2,6BP) for its activity. The Ka value of the enzyme for F2,6BP was 26 nᴍ. The Km values for fructose-6-phosphate (F6P) and sodium pyrophosphate (PPi), at physiological pH (7.2) in the presence of 1 µᴍ F2,6BP, were 0.59 mᴍ and 48 µᴍ, respectively. Intracellular levels of PPi and F6P varied from 17-71 nmol and from 37-65 nm per g fresh weight of the cells during culture. These results suggest that PPi-PFK is functional in Catharanthus roseus cells in vivo. The role of PPi-PFK in carbohydrate metabolism in heterotrophic, cultured plant cells is discussed.

scholarly journals Modeling and live imaging of mechanical instabilities in the zebrafish aorta during hematopoiesis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dmitrii Chalin ◽  
Charlotte Bureau ◽  
Andrea Parmeggiani ◽  
Sergei Rochal ◽  
Karima Kissa ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Axial Stress ◽  
Micromechanical Model ◽  
Model Organism ◽  
Complex Interplay ◽  
Hematopoietic Stem ◽  
Primary Model ◽  
Shape Changes

AbstractAll blood cells originate from hematopoietic stem/progenitor cells (HSPCs). HSPCs are formed from endothelial cells (ECs) of the dorsal aorta (DA), via endothelial-to-hematopoietic transition (EHT). The zebrafish is a primary model organism to study the process in vivo. While the role of mechanical stress in controlling gene expression promoting cell differentiation is actively investigated, mechanisms driving shape changes of the DA and individual ECs remain poorly understood. We address this problem by developing a new DA micromechanical model and applying it to experimental data on zebrafish morphogenesis. The model considers the DA as an isotropic tubular membrane subjected to hydrostatic blood pressure and axial stress. The DA evolution is described as a movement in the dimensionless controlling parameters space: normalized hydrostatic pressure and axial stress. We argue that HSPC production is accompanied by two mechanical instabilities arising in the system due to the plane stress in the DA walls and show how a complex interplay between mechanical forces in the system drives the emerging morphological changes.

scholarly journals Dark-Induced Barley Leaf Senescence – A Crop System for Studying Senescence and Autophagy Mechanisms

2021 ◽  
Vol 12 ◽  
Author(s):  
Ewelina Paluch-Lubawa ◽  
Ewelina Stolarska ◽  
Ewa Sobieszczuk-Nowicka
Keyword(s):  
Leaf Senescence ◽  
Control Mechanism ◽  
Morphological Changes ◽  
Plant Cells ◽  
Cell Components ◽  
Barley Leaf ◽  
Quality Control Mechanism ◽  
Crop System ◽  
Made In

This review synthesizes knowledge on dark-induced barley, attached, leaf senescence (DILS) as a model and discusses the possibility of using this crop system for studying senescence and autophagy mechanisms. It addresses the recent progress made in our understanding of DILS. The following aspects are discussed: the importance of chloroplasts as early targets of DILS, the role of Rubisco as the largest repository of recoverable nitrogen in leaves senescing in darkness, morphological changes of these leaves other than those described for chloroplasts and metabolic modifications associated with them, DILS versus developmental leaf senescence transcriptomic differences, and finally the observation that in DILS autophagy participates in the circulation of cell components and acts as a quality control mechanism during senescence. Despite the progression of macroautophagy, the symptoms of degradation can be reversed. In the review, the question also arises how plant cells regulate stress-induced senescence via autophagy and how the function of autophagy switches between cell survival and cell death.

scholarly journals Remodeling of cellular cytoskeleton by the acid sphingomyelinase/ceramide pathway

2008 ◽  
Vol 181 (2) ◽  
pp. 335-350 ◽  
Author(s):  
Youssef H. Zeidan ◽  
Russell W. Jenkins ◽  
Yusuf A. Hannun
Keyword(s):  
Morphological Changes ◽  
Acid Sphingomyelinase ◽  
Dominant Negative ◽  
Actin Binding ◽  
Cytoskeletal Remodeling ◽  
Membrane Protrusions ◽  
Exogenous Delivery ◽  
Cellular Cytoskeleton ◽  
Transient Elevation

The chemotherapeutic agent cisplatin is widely used in treatment of solid tumors. In breast cancer cells, cisplatin produces early and marked changes in cell morphology and the actin cytoskeleton. These changes manifest as loss of lamellipodia/filopodia and appearance of membrane ruffles. Furthermore, cisplatin induces dephosphorylation of the actin-binding protein ezrin, and its relocation from membrane protrusions to the cytosol. Because cisplatin activates acid sphingomyelinase (ASMase), we investigate here the role of the ASMase/ceramide (Cer) pathway in mediating these morphological changes. We find that cisplatin induces a transient elevation in ASMase activity and its redistribution to the plasma membrane. This translocation is blocked upon overexpression of a dominant-negative (DN) ASMaseS508A mutant and by a DN PKCδ. Importantly; knockdown of ASMase protects MCF-7 cells from cisplatin-induced cytoskeletal changes including ezrin dephosphorylation. Reciprocally, exogenous delivery of D-e-C16-Cer, but not dihydro-C16-Cer, recapitulates the morphotropic effects of cisplatin. Collectively, these results highlight a novel tumor suppressor property for Cer and a function for ASMase in cisplatin-induced cytoskeletal remodeling.

The function of S-nitrosothiols during abiotic stress in plants

2019 ◽  
Vol 70 (17) ◽  
pp. 4429-4439 ◽  
Author(s):  
Juan C Begara-Morales ◽  
Mounira Chaki ◽  
Raquel Valderrama ◽  
Capilla Mata-Pérez ◽  
Maria N Padilla ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Current Knowledge ◽  
Stomatal Closure ◽  
Cysteine Residue ◽  
Detection Methods ◽  
Plant Responses ◽  
Wide Range ◽  
Signaling Events

Abstract Nitric oxide (NO) is an active redox molecule involved in the control of a wide range of functions integral to plant biology. For instance, NO is implicated in seed germination, floral development, senescence, stomatal closure, and plant responses to stress. NO usually mediates signaling events via interactions with different biomolecules, for example the modulation of protein functioning through post-translational modifications (NO-PTMs). S-nitrosation is a reversible redox NO-PTM that consists of the addition of NO to a specific thiol group of a cysteine residue, leading to formation of S-nitrosothiols (SNOs). SNOs are more stable than NO and therefore they can extend and spread the in vivo NO signaling. The development of robust and reliable detection methods has allowed the identification of hundreds of S-nitrosated proteins involved in a wide range of physiological and stress-related processes in plants. For example, SNOs have a physiological function in plant development, hormone metabolism, nutrient uptake, and photosynthesis, among many other processes. The role of S-nitrosation as a regulator of plant responses to salinity and drought stress through the modulation of specific protein targets has also been well established. However, there are many S-nitrosated proteins that have been identified under different abiotic stresses for which the specific roles have not yet been identified. In this review, we examine current knowledge of the specific role of SNOs in the signaling events that lead to plant responses to abiotic stress, with a particular focus on examples where their functions have been well characterized at the molecular level.

scholarly journals The insulin sensitiser metformin regulates chicken Sertoli and germ cell populations

Reproduction ◽  
2016 ◽  
Vol 151 (5) ◽  
pp. 527-538 ◽  
Author(s):  
M Faure ◽  
E Guibert ◽  
S Alves ◽  
B Pain ◽  
C Ramé ◽  
...  
Keyword(s):  
Germ Cells ◽  
Sertoli Cells ◽  
Energy Content ◽  
Morphological Changes ◽  
Seminiferous Tubules ◽  
Reduce Food Intake ◽  
Testicular Weight

Abstract Metformin, an insulin sensitiser from the biguanide family of molecules, is used for the treatment of insulin resistance in type 2 diabetes individuals. It increases peripheral glucose uptake and may reduce food intake. Based on the tight link between metabolism and fertility, we investigated the role of metformin on testicular function using in vitro culture of Sertoli cells and seminiferous tubules, complemented by in vivo data obtained following metformin administration to prepubertal chickens. In vitro, metformin treatment reduced Sertoli cell proliferation without inducing apoptosis and morphological changes. The metabolism of Sertoli cells was affected because lactate secretion by Sertoli cells increased approximately twofold and intracellular free ATP was negatively impacted. Two important pathways regulating proliferation and metabolism in Sertoli cells were assayed. Metformin exposure was not associated with an increased phosphorylation of AKT or ERK. There was a 90% reduction in the proportion of proliferating germ cells after a 96-h exposure of seminiferous tubule cultures to metformin. In vivo, 6-week-old chickens treated with metformin for 3 weeks exhibited reduced testicular weight and a 50% decrease in testosterone levels. The expression of a marker of undifferentiated germ cells was unchanged in contrast to the decrease in expression of ‘protamine’, a marker of differentiated germ cells. In conclusion, these results suggest that metformin affects the testicular energy content and the proliferative ability of Sertoli and germ cells. Reproduction (2016) 151 527–538

scholarly journals Heterochromatin drives organization of conventional and inverted nuclei

2018 ◽  
Author(s):  
Martin Falk ◽  
Yana Feodorova ◽  
Natasha Naumova ◽  
Maxim Imakaev ◽  
Bryan R. Lajoie ◽  
...  
Keyword(s):  
Phase Separation ◽  
Morphological Changes ◽  
Nuclear Organization ◽  
Nuclear Periphery ◽  
Nuclear Architecture ◽  
Default State ◽  
Genomic Regions ◽  
Universal Mechanism

AbstractThe mammalian cell nucleus displays a remarkable spatial segregation of active euchromatic from inactive heterochromatic genomic regions. In conventional nuclei, euchromatin is localized in the nuclear interior and heterochromatin at the nuclear periphery. In contrast, rod photoreceptors in nocturnal mammals have inverted nuclei, with a dense heterochromatic core and a thin euchromatic outer shell. This inverted architecture likely converts rod nuclei into microlenses to facilitate nocturnal vision, and may relate to the absence of particular proteins that tether heterochromatin to the lamina. However, both the mechanism of inversion and the role of interactions between different types of chromatin and the lamina in nuclear organization remain unknown. To elucidate this mechanism we performed Hi-C and microscopy on cells with inverted nuclei and their conventional counterparts. Strikingly, despite the inversion evident in microscopy, both types of nuclei display similar Hi-C maps. To resolve this paradox we developed a polymer model of chromosomes and found a universal mechanism that reconciles Hi-C and microscopy for both inverted and conventional nuclei. Based solely on attraction between heterochromatic regions, this mechanism is sufficient to drive phase separation of euchromatin and heterochromatin and faithfully reproduces the 3D organization of inverted nuclei. When interactions between heterochromatin and the lamina are added, the same model recreates the conventional nuclear organization. To further test our models, we eliminated lamina interactions in models of conventional nuclei and found that this triggers a spontaneous process of inversion that qualitatively reproduces the pathway of morphological changes during nuclear inversion in vivo. Together, our experiments and modeling suggest that interactions among heterochromatic regions are central to phase separation of the active and inactive genome in inverted and conventional nuclei, while interactions with the lamina are essential for building the conventional architecture from these segregated phases. Ultimately our data suggest that an inverted organization constitutes the default state of nuclear architecture.

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