scholarly journals Pexophagy: The Selective Degradation of Peroxisomes

2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Andreas Till ◽  
Ronak Lakhani ◽  
Sarah F. Burnett ◽  
Suresh Subramani
Keyword(s):  
Mammalian Cells ◽  
Current Knowledge ◽  
Cell Types ◽  
Model Systems ◽  
Eukaryotic Cells ◽  
Organelle Biogenesis ◽  
Selective Degradation ◽  
Future Challenges ◽  
Recent Developments ◽  
Distinct Features

Peroxisomes are single-membrane-bounded organelles present in the majority of eukaryotic cells. Despite the existence of great diversity among different species, cell types, and under different environmental conditions, peroxisomes contain enzymes involved inβ-oxidation of fatty acids and the generation, as well as detoxification, of hydrogen peroxide. The exigency of all eukaryotic cells to quickly adapt to different environmental factors requires the ability to precisely and efficiently control peroxisome number and functionality. Peroxisome homeostasis is achieved by the counterbalance between organelle biogenesis and degradation. The selective degradation of superfluous or damaged peroxisomes is facilitated by several tightly regulated pathways. The most prominent peroxisome degradation system uses components of the general autophagy core machinery and is therefore referred to as “pexophagy.” In this paper we focus on recent developments in pexophagy and provide an overview of current knowledge and future challenges in the field. We compare different modes of pexophagy and mention shared and distinct features of pexophagy in yeast model systems, mammalian cells, and other organisms.

Mechanisms of Giardia lamblia differentiation into cysts

1997 ◽  
Vol 61 (3) ◽  
pp. 294-304
Author(s):  
H D Luján ◽  
M R Mowatt ◽  
T E Nash
Keyword(s):  
Giardia Lamblia ◽  
Current Knowledge ◽  
Regulation Of Gene Expression ◽  
Life Cycles ◽  
Eukaryotic Cells ◽  
Organelle Biogenesis ◽  
Adaptive Responses ◽  
Specific Stimulus ◽  
Adverse Conditions

Microbiologists have long been intrigued by the ability of parasitic organisms to adapt to changes in the environment. Since most parasites occupy several niches during their journey between vectors and hosts, they have developed adaptive responses which allow them to survive under adverse conditions. Therefore, the life cycles of protozoan and helminthic parasites are excellent models with which to study numerous mechanisms involved in cell differentiation, such as the regulation of gene expression, signal transduction pathways, and organelle biogenesis. Unfortunately, many of these studies are very difficult because the conditions needed to elicit developmental changes in parasites remain undetermined in most cases. Recently, several interesting findings were reported on the process of differentiation of Giardia lamblia trophozoites into cysts. G. lamblia is a flagellated protozoan that inhabits the upper small intestine of its vertebrate host and is a major cause of enteric disease worldwide. It belongs to the earliest identified lineage among eukaryotes and therefore offers a unique insight into the progression from primitive to more complex eukaryotic cells. The discovery of a specific stimulus that induces trophozoites to differentiate into cysts, the identification and characterization of encystation-specific molecules, the elucidation of novel biochemical pathways, and the development of useful reagents and techniques have made this parasite an excellent model with which to study differentiation in eukaryotic cells. In this review, we summarize the most recent fundings on several aspects of Giardia differentiation and discuss the significance of these findings within the context of current knowledge in the field.

scholarly journals Microtubules support a disk-like septin arrangement at the plasma membrane of mammalian cells

2011 ◽  
Vol 22 (23) ◽  
pp. 4588-4601 ◽  
Author(s):  
Mikael E. Sellin ◽  
Per Holmfeldt ◽  
Sonja Stenmark ◽  
Martin Gullberg
Keyword(s):  
Plasma Membrane ◽  
Mammalian Cells ◽  
Cell Model ◽  
Cell Types ◽  
Higher Order ◽  
Model Systems ◽  
Animal Cells ◽  
Endogenous Gene ◽  
Binding Domains ◽  
Substrate Adhesion

Septin family proteins oligomerize through guanosine 5′-triphosphate–binding domains into core heteromers, which in turn polymerize at the cleavage furrow of dividing fungal and animal cells. Septin assemblies during the interphase of animal cells remain poorly defined and are the topic of this report. In this study, we developed protocols for visualization of authentic higher-order assemblies using tagged septins to effectively replace the endogenous gene product within septin core heteromers in human cells. Our analysis revealed that septins assemble into microtubule-supported, disk-like structures at the plasma membrane. In the absence of cell substrate adhesion, this is the predominant higher-order arrangement in interphase cells and each of the seven to eight septin family members expressed by the two analyzed cell types appears equally represented. However, studies of myeloid and lymphoid cell model systems revealed cell type–specific alterations of higher-order septin arrangements in response to substrate adhesion. Live-cell observations suggested that all higher-order septin assemblies are mutually exclusive with plasma membrane regions undergoing remodeling. The combined data point to a mechanism by which densely arranged cortical microtubules, which are typical for nonadhered spherical cells, support plasma membrane–bound, disk-like septin assemblies.

Nanomedicine for Cancer Therapy Using Autophagy: An Overview

2019 ◽  
Vol 18 (30) ◽  
pp. 2599-2613 ◽  
Author(s):  
Rajesh Kotcherlakota ◽  
Syed Tazib Rahaman ◽  
Chitta Ranjan Patra
Keyword(s):  
Cancer Therapy ◽  
Mammalian Cells ◽  
Clinical Status ◽  
Alpha Synuclein ◽  
Review Article ◽  
Tau Proteins ◽  
Present Review ◽  
Alternative Treatment Option ◽  
Future Challenges ◽  
Recent Developments

Autophagy is an intracellular biological catabolic process of mammalian cells to maintain the homeostasis. It plays a wide role in the clearance of damaged cellular organelles, misfolded or aggregated proteins like alpha-synuclein, β-amyloid peptides, Tau proteins and pathogens. Recent studies have clearly demonstrated that dysfunction in autophagy leads to the development of cancer, cardiomyopathy, chronic infection, neurodegenerative and other diseases. Therefore, modulation of autophagy has therapeutic value to cure the diseases including cancer using external stimuli. In this context, various researchers developed small molecules such as chloroquine, rapamycin, etc. for the treatment of cancer through autophagy. However, these molecules possess side effects which limit their use in the clinics. Therefore, nanomedicine approach could stand as an alternative treatment option to induce the autophagy in cancer therapy. Several investigators developed a variety of nanomaterials which themselves act as autophagy inducers or inhibitors. Considering this, the present review article will focus on the recent developments of nanomedicine in the area of autophagy that have been focused on the treatment of cancers. We also summarised the detailed mechanisms of nanoparticles mediated autophagy which could be helpful for developing new strategies to fight against cancer. Also, the present review article covers the current clinical status of nanomedicine and future challenges. Finally, we conclude with the future potential role of nanomedicine for autophagy induction in the cancer treatment.

Neuronal calcium sensor-1: a multifunctional regulator of secretion

2003 ◽  
Vol 31 (4) ◽  
pp. 828-832 ◽  
Author(s):  
S. Hilfiker
Keyword(s):  
Guanylate Cyclase ◽  
Neurotransmitter Release ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Photoreceptor Cells ◽  
Cell Types ◽  
Dependent Manner ◽  
Calcium Sensor ◽  
Neuronal Calcium Sensor

Ca2+ ions play a crucial role not only as the trigger for neurotransmitter release, but also in other aspects of brain function, such as short-term and long-term modulation of synaptic efficacy, which may underlie certain forms of learning and memory. The actions of Ca2+ are mediated by Ca2+-binding proteins, including a group of proteins known as neuronal calcium sensor (NCS) proteins. The NCS family includes NCS-1, visinin-like proteins, recoverins, guanylate cyclase-activating proteins and potassium channel-interacting proteins. Some members of this family, such as recoverin and guanylate cyclase-activating protein, are only expressed in photoreceptor cells and have been implicated in the control of visual transduction pathways, while the functional roles of the other members are largely unknown. NCS-1 was originally identified in Drosophila in a screen for neuronal hyperexcitability mutants. NCS-1 is an N-terminally myristoylated protein that contains four EF-hand motifs, three of which are able to bind Ca2+ in the submicromolar range. Overexpression of NCS-1 has been shown to enhance evoked neurotransmitter release, paired-pulse facilitation and exocytosis in several neuronal and neuroendocrine cell types. Recent experiments suggest that NCS-1 interacts directly with phosphatidylinositol 4-hydroxykinase in yeast as well as mammalian cells, suggesting that it may enhance neuronal secretion by modulating cellular trafficking steps in a phosphoinositide-dependent manner. In contrast, an involvement of NCS-1 in the expression and regulation of voltage-gated Ca2+ channels and K+ channels has also been proposed, which may be attributed, at least in part, to the effects of NCS-1 on vesicular trafficking pathways. The present review describes current knowledge about the cellular functions and molecular mechanisms by which NCS-1 may regulate neurotransmitter release.

scholarly journals Degron-tagged reporters probe membrane topology and enable the specific labelling of membrane-wrapped structures

2018 ◽  
Author(s):  
Katharina B Beer ◽  
Gholamreza Fazeli ◽  
Kristyna Judasova ◽  
Linda Irmisch ◽  
Jona Causemann ◽  
...  
Keyword(s):  
Mammalian Cells ◽  
Membrane Topology ◽  
Model Systems ◽  
C Elegans ◽  
Selective Degradation ◽  
Multiple Structures ◽  
Cell Fragments ◽  
Specific Membrane ◽  
Specific Labelling

AbstractVisualization of specific organelles in tissues over background fluorescence can be challenging, especially when reporters localize to multiple structures. Instead of trying to identify proteins enriched in specific membrane-wrapped structures, we used a selective degradation approach to remove reporters from the cytoplasm or nucleus of C. elegans embryos and mammalian cells. We demonstrate specific labelling of organelles using degron-tagged reporters, including extracellular vesicles, as well as individual neighbouring membranes. These degron-tagged reporters facilitate long-term tracking of released cell debris and cell corpses, even during uptake and phagolysosomal degradation. We further show that degron protection assays can probe the topology of the nuclear envelope and plasma membrane during cell division, giving insight into protein and organelle dynamics. As endogenous and heterologous degrons are used in bacteria, yeast, plants, and animals, degron approaches can enable the specific labelling and tracking of proteins, vesicles, organelles, cell fragments, and cells in many model systems.

Ultrastructural Changes in Three Different Mammalian Cells Following Ultraviolet Laser Irradiation

1972 ◽  
Vol 30 ◽  
pp. 350-351
Author(s):  
K. Shankar Narayan ◽  
Kailash C. Gupta ◽  
Tohru Okigaki
Keyword(s):  
Ultraviolet Light ◽  
Mammalian Cells ◽  
Biological Effects ◽  
Survival Rates ◽  
Chinese Hamster ◽  
Cell Types ◽  
Differential Sensitivity ◽  
Ultrastructural Changes ◽  
Ultraviolet Laser

The biological effects of short-wave ultraviolet light has generally been described in terms of changes in cell growth or survival rates and production of chromosomal aberrations. Ultrastructural changes following exposure of cells to ultraviolet light, particularly at 265 nm, have not been reported.We have developed a means of irradiating populations of cells grown in vitro to a monochromatic ultraviolet laser beam at a wavelength of 265 nm based on the method of Johnson. The cell types studies were: i) WI-38, a human diploid fibroblast; ii) CMP, a human adenocarcinoma cell line; and iii) Don C-II, a Chinese hamster fibroblast cell strain. The cells were exposed either in situ or in suspension to the ultraviolet laser (UVL) beam. Irradiated cell populations were studied either "immediately" or following growth for 1-8 days after irradiation.Differential sensitivity, as measured by survival rates were observed in the three cell types studied. Pattern of ultrastructural changes were also different in the three cell types.

Noncoding RNAs in Medicinal Plants and Their Regulatory Roles in Bioactive Compound Production

2020 ◽  
Vol 21 ◽  
Author(s):  
Caili Li ◽  
Meizhen Wang ◽  
Xiaoxiao Qiu ◽  
Hong Zhou ◽  
Shanfa Lu
Keyword(s):  
Medicinal Plants ◽  
Current Knowledge ◽  
Salvia Miltiorrhiza ◽  
Noncoding Rnas ◽  
Bioactive Compound ◽  
Research Field ◽  
Model Systems ◽  
Small Interfering Rnas ◽  
Regulatory Pathways ◽  
Regulatory Modules

Background: Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs), small interfering RNAs (siRNAs) and long noncoding RNAs (lncRNAs), play significant regulatory roles in plant development and secondary metabolism and are involved in plant response to biotic and abiotic stresses. They have been intensively studied in model systems and crops for approximately two decades and massive amount of information have been obtained. However, for medicinal plants, ncRNAs, particularly their regulatory roles in bioactive compound biosynthesis, are just emerging as a hot research field. Objective: This review aims to summarize current knowledge on herbal ncRNAs and their regulatory roles in bioactive compound production. Results and Conclusion: So far, scientists have identified thousands of miRNA candidates from over 50 medicinal plant species and 11794 lncRNAs from Salvia miltiorrhiza, Panax ginseng, and Digitalis purpurea. Among them, more than 30 miRNAs and five lncRNAs have been predicted to regulate bioactive compound production. The regulation may achieve through various regulatory modules and pathways, such as the miR397-LAC module, the miR12112-PPO module, the miR156-SPL module, the miR828-MYB module, the miR858-MYB module, and other siRNA and lncRNA regulatory pathways. Further functional analysis of herbal ncRNAs will provide useful information for quality and quantity improvement of medicinal plants.

Role of inflammation in the development of colorectal cancer

2020 ◽  
Vol 20 ◽  
Author(s):  
Sridhar Muthusami ◽  
R. Ileng Kumaran ◽  
Kokelavani Nampalli Babu ◽  
Sneha Krishnamoorthy ◽  
Akash Guruswamy ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Interleukin 1 ◽  
Cell Types ◽  
Model Systems ◽  
Cytokine Gene Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Molecules

: Chronic inflammation can lead to the development of many diseases including cancer. Inflammatory bowel disease (IBD) that includes both ulcerative colitis (UC) and Crohn's disease (CD) are risk factors for the development of colorectal cancer (CRC). Many cytokines produced primarily by the gut immune cells either during or in response to localized inflammation in the colon and rectum are known to stimulate the complex interactions between the different cell types in the gut environment resulting in acute inflammation. Subsequently, chronic inflammation together with genetic and epigenetic changes has been shown to lead to the development and progression of CRC. Various cell types present in the colon such as enterocytes, Paneth cells, goblet cells and macrophages express receptors for inflammatory cytokines and respond to tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and other cytokines. Among the several cytokines produced, TNF-α and IL-1β are the key proinflammatory molecules that play critical roles in the development of CRC. The current review is intended to consolidate the published findings to focus on the role of proinflammatory cytokines, namely TNF-α and IL-1β, on inflammation (and the altered immune response) in the gut, to better understand the development of CRC in IBD, using various experimental model systems, preclinical and clinical studies. Moreover, this review also highlights the current therapeutic strategies available (monotherapy and combination therapy), to alleviate the symptoms or treat inflammationassociated CRC by using monoclonal antibodies or aptamers to block proinflammatory molecules, inhibitors of tyrosine kinases in inflammatory signaling cascade, competitive inhibitors of proinflammatory molecules, and the nucleic acid drugs like small activating RNAs (saRNAs) or microRNA (miRNA) mimics to activate tumor suppressor or repress oncogene/proinflammatory cytokine gene expression.

scholarly journals Hypoxia, Acidification and Inflammation: Partners in Crime in Parkinson’s Disease Pathogenesis?

Immuno ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 78-90
Author(s):  
Johannes Burtscher ◽  
Grégoire P. Millet
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Current Knowledge ◽  
Cell Types ◽  
Brain Cell ◽  
Special Focus ◽  
Molecular Alterations ◽  
Research Fields

Like in other neurodegenerative diseases, protein aggregation, mitochondrial dysfunction, oxidative stress and neuroinflammation are hallmarks of Parkinson’s disease (PD). Differentiating characteristics of PD include the central role of α-synuclein in the aggregation pathology, a distinct vulnerability of the striato-nigral system with the related motor symptoms, as well as specific mitochondrial deficits. Which molecular alterations cause neurodegeneration and drive PD pathogenesis is poorly understood. Here, we summarize evidence of the involvement of three interdependent factors in PD and suggest that their interplay is likely a trigger and/or aggravator of PD-related neurodegeneration: hypoxia, acidification and inflammation. We aim to integrate the existing knowledge on the well-established role of inflammation and immunity, the emerging interest in the contribution of hypoxic insults and the rather neglected effects of brain acidification in PD pathogenesis. Their tight association as an important aspect of the disease merits detailed investigation. Consequences of related injuries are discussed in the context of aging and the interaction of different brain cell types, in particular with regard to potential consequences on the vulnerability of dopaminergic neurons in the substantia nigra. A special focus is put on the identification of current knowledge gaps and we emphasize the importance of related insights from other research fields, such as cancer research and immunometabolism, for neurodegeneration research. The highlighted interplay of hypoxia, acidification and inflammation is likely also of relevance for other neurodegenerative diseases, despite disease-specific biochemical and metabolic alterations.

scholarly journals Glucocorticoid Receptor β (GRβ): Beyond Its Dominant-Negative Function

2021 ◽  
Vol 22 (7) ◽  
pp. 3649
Author(s):  
Patricia Ramos-Ramírez ◽  
Omar Tliba
Keyword(s):  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Cell Communication ◽  
Cell Types ◽  
The Body ◽  
Dominant Negative ◽  
Negative Effects ◽  
Independent Manner ◽  
Distinct Cell ◽  
Induced Apoptosis

Glucocorticoids (GCs) act via the GC receptor (GR), a receptor ubiquitously expressed in the body where it drives a broad spectrum of responses within distinct cell types and tissues, which vary in strength and specificity. The variability of GR-mediated cell responses is further extended by the existence of GR isoforms, such as GRα and GRβ, generated through alternative splicing mechanisms. While GRα is the classic receptor responsible for GC actions, GRβ has been implicated in the impairment of GRα-mediated activities. Interestingly, in contrast to the popular belief that GRβ actions are restricted to its dominant-negative effects on GRα-mediated responses, GRβ has been shown to have intrinsic activities and “directly” regulates a plethora of genes related to inflammatory process, cell communication, migration, and malignancy, each in a GRα-independent manner. Furthermore, GRβ has been associated with increased cell migration, growth, and reduced sensitivity to GC-induced apoptosis. We will summarize the current knowledge of GRβ-mediated responses, with a focus on the GRα-independent/intrinsic effects of GRβ and the associated non-canonical signaling pathways. Where appropriate, potential links to airway inflammatory diseases will be highlighted.

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