scholarly journals Cadmium-Induced Cell Homeostasis Impairment is Suppressed by the Tor1 Deficiency in Fission Yeast

2020 ◽  
Vol 21 (21) ◽  
pp. 7847
Author(s):  
Miroslava Požgajová ◽  
Alica Navrátilová ◽  
Eva Šebová ◽  
Marek Kovár ◽  
Miroslava Kačániová
Keyword(s):  
Fission Yeast ◽  
Inductively Coupled Plasma ◽  
Defense Mechanisms ◽  
Model Organism ◽  
Optical Emission ◽  
The Body ◽  
Wild Type ◽  
Cd Uptake ◽  
Underlying Mechanisms

Cadmium has no known physiological function in the body; however, its adverse effects are associated with cancer and many types of organ system damage. Although much has been shown about Cd toxicity, the underlying mechanisms of its responses to the organism remain unclear. In this study, the role of Tor1, a catalytic subunit of the target of rapamycin complex 2 (TORC2), in Cd-mediated effects on cell proliferation, the antioxidant system, morphology, and ionome balance was investigated in the eukaryotic model organism Schizosaccharomyces pombe. Surprisingly, spectrophotometric and biochemical analyses revealed that the growth rate conditions and antioxidant defense mechanisms are considerably better in cells lacking the Tor1 signaling. The malondialdehyde (MDA) content of Tor1-deficient cells upon Cd treatment represents approximately half of the wild-type content. The microscopic determination of the cell morphological parameters indicates the role for Tor1 in cell shape maintenance. The ion content, determined by inductively coupled plasma optical emission spectroscopy (ICP-OES), showed that the Cd uptake potency was markedly lower in Tor1-depleted compared to wild-type cells. Conclusively, we show that the cadmium-mediated cell impairments in the fission yeast significantly depend on the Tor1 signaling. Additionally, the data presented here suggest the yet-undefined role of Tor1 in the transport of ions.

scholarly journals Catalase T-Deficient Fission Yeast Meiocytes Show Resistance to Ionizing Radiation

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 881 ◽  
Author(s):  
Razan Muhtadi ◽  
Alexander Lorenz ◽  
Samantha J. Mpaulo ◽  
Christian Siebenwirth ◽  
Harry Scherthan
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Ionizing Radiation ◽  
Fission Yeast ◽  
Defense Mechanisms ◽  
Meiotic Chromosome ◽  
Premature Aging ◽  
Wild Type ◽  
Moderate Sensitivity

Environmental stress, reactive oxygen species (ROS), or ionizing radiation (IR) can induce adverse effects in organisms and their cells, including mutations and premature aging. DNA damage and its faulty repair can lead to cell death or promote cancer through the accumulation of mutations. Misrepair in germ cells is particularly dangerous as it may lead to alterations in developmental programs and genetic disease in the offspring. DNA damage pathways and radical defense mechanisms mediate resistance to genotoxic stresses. Here, we investigated, in the fission yeast Schizosaccharomyces pombe, the role of the H2O2-detoxifying enzyme cytosolic catalase T (Ctt1) and the Fe2+/Mn2+ symporter Pcl1 in protecting meiotic chromosome dynamics and gamete formation from radicals generated by ROS and IR. We found that wild-type and pcl1-deficient cells respond similarly to X ray doses of up to 300 Gy, while ctt1∆ meiocytes showed a moderate sensitivity to IR but a hypersensitivity to hydrogen peroxide with cells dying at >0.4 mM H2O2. Meiocytes deficient for pcl1, on the other hand, showed a resistance to hydrogen peroxide similar to that of the wild type, surviving doses >40 mM. In all, it appears that in the absence of the main H2O2-detoxifying pathway S. pombe meiocytes are able to survive significant doses of IR-induced radicals.

scholarly journals Migration of Silver and Copper Nanoparticles from Food Coating

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 380
Author(s):  
Hamed Ahari ◽  
Leila Khoshboui Lahijani
Keyword(s):  
Copper Nanoparticles ◽  
Inductively Coupled Plasma ◽  
Food Packaging ◽  
Human Life ◽  
Analytical Techniques ◽  
Optical Emission ◽  
Atomic Emission ◽  
The Body ◽  
Toxic Effects ◽  
Inductively Coupled

Packaging containing nanoparticles (NPs) can increase the shelf life of products, but the presence of NPs may hazards human life. In this regard, there are reports regarding the side effect and cytotoxicity of nanoparticles. The main aim of this research was to study the migration of silver and copper nanoparticles from the packaging to the food matrix as well as the assessment techniques. The diffusion and migration of nanoparticles can be analyzed by analytical techniques including atomic absorption, inductively coupled plasma mass spectrometry, inductively coupled plasma atomic emission, and inductively coupled plasma optical emission spectroscopy, as well as X-ray diffraction, spectroscopy, migration, and titration. Inductively coupled plasma-based techniques demonstrated the best results. Reports indicated that studies on the migration of Ag/Cu nanoparticles do not agree with each other, but almost all studies agree that the migration of these nanoparticles is higher in acidic environments. There are widespread ambiguities about the mechanism of nanoparticle toxicity, so understanding these nanoparticles and their toxic effects are essential. Nanomaterials that enter the body in a variety of ways can be distributed throughout the body and damage human cells by altering mitochondrial function, producing reactive oxygen, and increasing membrane permeability, leading to toxic effects and chronic disease. Therefore, more research needs to be done on the development of food packaging coatings with consideration given to the main parameters affecting nanoparticles migration.

Touch insensitive foraging of Caenorhabditis elegans in a constrained structure

Nematology ◽  
2009 ◽  
Vol 11 (4) ◽  
pp. 551-554
Author(s):  
Jinu Eo ◽  
Kazunori Otobe
Keyword(s):  
Caenorhabditis Elegans ◽  
Natural Habitat ◽  
The Body ◽  
Wild Type ◽  
Agar Gel ◽  
Touch Sensor ◽  
Foraging Pattern

Abstract The objective of this study was to clarify the role of touch sensors in the foraging of Caenorhabditis elegans in a constrained structure. The strains tested included an array of mechanosensory mutants insensitive to touch in the body, tail or nose. The mutants and wild type nematodes repeated forward and backward movement in a micro-moulded substrate as on the surface of agar gel. Differences in the foraging pattern were not obvious among mutant groups having different touch sensor deficit in the substrate, and all strains of nematode successfully moved out of the T-shaped structure after searching the configuration of their environment. The results suggest that the touch sensor is a weak contributor to the performance of the worms when foraging, and the behaviour is governed by intrinsic spontaneous patterns in the absence of any stimuli in natural habitat.

scholarly journals Review: The Role of Wnt/β-Catenin Signalling in Neural Crest Development in Zebrafish

2021 ◽  
Vol 9 ◽  
Author(s):  
Gemma Sutton ◽  
Robert N. Kelsh ◽  
Steffen Scholpp
Keyword(s):  
Neural Crest ◽  
Pigment Cell ◽  
Model Organism ◽  
Neural Plate ◽  
The Body ◽  
Signalling Pathway ◽  
Border Region ◽  
Pigment Cells ◽  
Neural Plate Border

The neural crest (NC) is a multipotent cell population in vertebrate embryos with extraordinary migratory capacity. The NC is crucial for vertebrate development and forms a myriad of cell derivatives throughout the body, including pigment cells, neuronal cells of the peripheral nervous system, cardiomyocytes and skeletogenic cells in craniofacial tissue. NC induction occurs at the end of gastrulation when the multipotent population of NC progenitors emerges in the ectodermal germ layer in the neural plate border region. In the process of NC fate specification, fate-specific markers are expressed in multipotent progenitors, which subsequently adopt a specific fate. Thus, NC cells delaminate from the neural plate border and migrate extensively throughout the embryo until they differentiate into various cell derivatives. Multiple signalling pathways regulate the processes of NC induction and specification. This review explores the ongoing role of the Wnt/β-catenin signalling pathway during NC development, focusing on research undertaken in the Teleost model organism, zebrafish (Danio rerio). We discuss the function of the Wnt/β-catenin signalling pathway in inducing the NC within the neural plate border and the specification of melanocytes from the NC. The current understanding of NC development suggests a continual role of Wnt/β-catenin signalling in activating and maintaining the gene regulatory network during NC induction and pigment cell specification. We relate this to emerging models and hypotheses on NC fate restriction. Finally, we highlight the ongoing challenges facing NC research, current gaps in knowledge, and this field’s potential future directions.

scholarly journals Role of ROS in ischemia-induced lung angiogenesis

2010 ◽  
Vol 299 (4) ◽  
pp. L535-L541 ◽  
Author(s):  
Julie Nijmeh ◽  
Aigul Moldobaeva ◽  
Elizabeth M. Wagner
Keyword(s):  
Pulmonary Artery ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Wild Type ◽  
Systemic Blood Flow ◽  
Artery Ligation ◽  
Underlying Mechanisms ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction

Pulmonary artery obstruction and subsequent lung ischemia have been shown to induce systemic angiogenesis despite preservation of normoxia. The underlying mechanisms, however, remain poorly understood. In a mouse model of lung ischemia induced by left pulmonary artery ligation (LPAL), we showed previously, the formation of a new systemic vasculature to the ischemic lung. We hypothesize that LPAL in the mouse increases reactive oxygen species (ROS) production, and these molecules play an initiating role in subsequent lung neovascularization. We used oxidant-sensitive dyes (DHE and H2DCF-DA) to quantify ROS and measured the antioxidant-reduced glutathione (GSH) and its oxidized form (GSSG) as indicators of ROS levels after LPAL. The magnitude of systemic neovascularization was determined by measuring systemic blood flow to the left lung with radiolabeled microspheres 14 days after LPAL. An increase in ROS was observed early (30 min: 55% increase in H2DCF-DA) after LPAL, with a return to baseline by 24 h. GSH/GSSG was decreased (∼50%) 4 h after LPAL, suggesting earlier ROS upregulation. Mice treated with the antioxidant N-acetylcysteine showed attenuated angiogenesis (62% of wild-type LPAL), and mice lacking Nrf2, a transcription factor important for antioxidant synthesis, resulted in increased neovascularization (207% of wild-type LPAL). Overall, GSH/GSSG was inversely associated with the magnitude of neovascularization. These results demonstrate that LPAL induces an early and transient ROS upregulation, and ROS appear to play a role in promoting ischemia-induced angiogenesis.

Apical-basal pattern formation in the Arabidopsis embryo: studies on the role of the gnom gene

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 149-162 ◽  
Author(s):  
U. Mayer ◽  
G. Buttner ◽  
G. Jurgens
Keyword(s):  
Pattern Formation ◽  
Root Formation ◽  
Asymmetric Cell Division ◽  
Early Embryo ◽  
The Body ◽  
Wild Type ◽  
Early Effect ◽  
Normal Number ◽  
Mutant Seedling

gnom is one of several genes that make substantial contributions to pattern formation along the apical-basal axis of polarity in the Arabidopsis embryo as indicated by the mutant seedling phenotype. The apical and basal end regions of the body pattern, which include the meristems of the shoot and the root, fail to form, and a minority of mutant embryos lack morphological features of apical-basal polarity. We have investigated the developmental basis of the gnom mutant phenotype, taking advantage of a large number of EMS-induced mutant alleles. The seedling phenotype has been traced back to the early embryo in which the asymmetric division of the zygote is altered, now producing two nearly equal-sized cells. The apical daughter cell then undergoes abnormal divisions, resulting in an octant embryo with about twice the normal number of cells while the uppermost derivative of the basal cell fails to become the hypophysis, which normally contributes to root development. Consistent with this early effect, gnom appears to be epistatic to monopteros in doubly mutant embryos, suggesting that, without prior gnom activity, the monopteros gene cannot promote root and hypocotyl development. On the other hand, when root formation was induced in bisected seedlings, wild-type responded whereas gnom mutants failed to produce a root but formed callus instead. These results suggest that gnom activity promotes asymmetric cell division which we believe is necessary both for apical-basal pattern formation in the early embryo and for root formation in tissue culture.

scholarly journals Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection

2007 ◽  
Vol 75 (6) ◽  
pp. 3055-3061 ◽  
Author(s):  
Xiaowen L. Rudner ◽  
Kyle I. Happel ◽  
Erana A. Young ◽  
Judd E. Shellito
Keyword(s):  
T Cells ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Pneumocystis Carinii ◽  
Neutralizing Antibody ◽  
Wild Type ◽  
Pneumocystis Carinii Infection ◽  
Interleukin 23

ABSTRACT Host defense mechanisms against Pneumocystis carinii are not fully understood. Previous work in the murine model has shown that host defense against infection is critically dependent upon host CD4+ T cells. The recently described Th17 immune response is predominantly a function of effector CD4+ T cells stimulated by interleukin-23 (IL-23), but whether these cells are required for defense against P. carinii infection is unknown. We tested the hypothesis that P. carinii stimulates the early release of IL-23, leading to increases in IL-17 production and lung effector CD4+ T-cell population that mediate clearance of infection. In vitro, stimulation of alveolar macrophages with P. carinii induced IL-23, and IL-23p19 mRNA was expressed in lungs of mice infected with this pathogen. To address the role of IL-23 in resistance to P. carinii, IL-23p19−/− and wild-type control C57BL/6 mice were infected and their fungal burdens and cytokine/chemokine responses were compared. IL-23p19−/− mice displayed transient but impaired clearance of infection, which was most apparent 2 weeks after inoculation. In confirmatory studies, the administration of either anti-IL-23p19 or anti-IL-17 neutralizing antibody to wild-type mice infected with P. carinii also caused increases in fungal burdens. IL-17 and the lymphocyte chemokines IP-10, MIG, MIP-1α, MIP-1β, and RANTES were decreased in the lungs of infected IL-23p19−/− mice in comparison to their levels in the lungs of wild-type mice. In IL-23p19−/− mice infected with P. carinii, there were fewer effector CD4+ T cells in the lung tissue. Collectively, these studies indicate that the IL-23-IL-17 axis participates in host defense against P. carinii.

scholarly journals Role of CheB and CheR in the Complex Chemotactic and Aerotactic Pathway of Azospirillum brasilense

2006 ◽  
Vol 188 (13) ◽  
pp. 4759-4768 ◽  
Author(s):  
Bonnie B. Stephens ◽  
Star N. Loar ◽  
Gladys Alexandre
Keyword(s):  
Escherichia Coli ◽  
Steady State ◽  
Azospirillum Brasilense ◽  
Model Organism ◽  
Spatial Gradient ◽  
Wild Type ◽  
Temporal Gradient ◽  
E Coli ◽  
Significant Difference

ABSTRACT It has previously been reported that the alpha-proteobacterium Azospirillum brasilense undergoes methylation-independent chemotaxis; however, a recent study revealed cheB and cheR genes in this organism. We have constructed cheB, cheR, and cheBR mutants of A. brasilense and determined that the CheB and CheR proteins under study significantly influence chemotaxis and aerotaxis but are not essential for these behaviors to occur. First, we found that although cells lacking CheB, CheR, or both were no longer capable of responding to the addition of most chemoattractants in a temporal gradient assay, they did show a chemotactic response (albeit reduced) in a spatial gradient assay. Second, in comparison to the wild type, cheB and cheR mutants under steady-state conditions exhibited an altered swimming bias, whereas the cheBR mutant and the che operon mutant did not. Third, cheB and cheR mutants were null for aerotaxis, whereas the cheBR mutant showed reduced aerotaxis. In contrast to the swimming bias for the model organism Escherichia coli, the swimming bias in A. brasilense cells was dependent on the carbon source present and cells released methanol upon addition of some attractants and upon removal of other attractants. In comparison to the wild type, the cheB, cheR, and cheBR mutants showed various altered patterns of methanol release upon exposure to attractants. This study reveals a significant difference between the chemotaxis adaptation system of A. brasilense and that of the model organism E. coli and suggests that multiple chemotaxis systems are present and contribute to chemotaxis and aerotaxis in A. brasilense.

scholarly journals Expression of the cytoplasmic NPM1 mutant (NPMc+) causes the expansion of hematopoietic cells in zebrafish

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3329-3340 ◽  
Author(s):  
Niccolò Bolli ◽  
Elspeth M. Payne ◽  
Clemens Grabher ◽  
Jeong-Soo Lee ◽  
Adam B. Johnston ◽  
...  
Keyword(s):  
Hematopoietic Cells ◽  
Model Organism ◽  
Myeloid Cell ◽  
Wild Type ◽  
Zebrafish Model ◽  
Blood Island ◽  
Cell Numbers ◽  
Myeloid Leukemias ◽  
Underlying Mechanisms ◽  
Ventral Wall

AbstractMutations in the human nucleophosmin (NPM1) gene are the most frequent genetic alteration in adult acute myeloid leukemias (AMLs) and result in aberrant cytoplasmic translocation of this nucleolar phosphoprotein (NPMc+). However, underlying mechanisms leading to leukemogenesis remain unknown. To address this issue, we took advantage of the zebrafish model organism, which expresses 2 genes orthologous to human NPM1, referred to as npm1a and npm1b. Both genes are ubiquitously expressed, and their knockdown produces a reduction in myeloid cell numbers that is specifically rescued by NPM1 expression. In zebrafish, wild-type human NPM1 is nucleolar while NPMc+ is cytoplasmic, as in human AML, and both interact with endogenous zebrafish Npm1a and Npm1b. Forced NPMc+ expression in zebrafish causes an increase in pu.1+ primitive early myeloid cells. A more marked perturbation of myelopoiesis occurs in p53m/m embryos expressing NPMc+, where mpx+ and csf1r+ cell numbers are also expanded. Importantly, NPMc+ expression results in increased numbers of definitive hematopoietic cells, including erythromyeloid progenitors in the posterior blood island and c-myb/cd41+ cells in the ventral wall of the aorta. These results are likely to be relevant to human NPMc+ AML, where the observed NPMc+ multilineage expression pattern implies transformation of a multipotent stem or progenitor cell.

scholarly journals The dgc2 gene encoding di-guanylate cyclase suppresses both motility and biofilm formation in the filamentous cyanobacterium Leptolyngbya boryana.

2022 ◽  
Author(s):  
Kazuma Toida ◽  
Wakana Kushida ◽  
Hiroki Yamamoto ◽  
Kyoka Yamamoto ◽  
Kazuma Uesaka ◽  
...  
Keyword(s):  
Mutant Strain ◽  
Biofilm Formation ◽  
Catalytic Domain ◽  
Genetic Model ◽  
Model Organism ◽  
Gliding Motility ◽  
Spontaneous Mutant ◽  
Filamentous Cyanobacterium ◽  
Wild Type

Colony pattern formations of bacteria with motility manifest complicated morphological self-organization phenomena. Leptolyngbya boryana is the filamentous cyanobacterial species, which has been used as a genetic model organism for studying metabolism including photosynthesis and nitrogen-fixation. Although a widely used type strain (wild type) of this species has not been reported to show any motile activity, we isolated a spontaneous mutant strain which shows active motility (gliding activity) to give rise to complicated colony patters, including comet-like wandering clusters and disk-like rotating vortices on solid media. Whole-genome resequencing identified multiple mutations on the genome in the mutant strain. We confirmed that inactivation of a candidate gene, dgc2 (LBDG_02920), in the wild type background was sufficient to give rise to motility and the morphological colony patterns. This gene encodes a protein, containing the GGDEF motif, which is conserved at the catalytic domain of diguanylate cyclase (DGC). Although DGC has been reported to be involved in biofilm formation, the mutant strain lacking dgc2 significantly facilitated biofilm formation, suggesting a role of DGC for suppressing both gliding motility and biofilm formation. Thus, L. boryana provides an excellent genetic model to study dynamic colony pattern formation, and novel insight on a role of c-di-GMP for biofilm formation.

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