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Cell Organelles (cell + organelle)
Selected AbstractsThe role of mitochondria in inherited neurodegenerative diseasesJOURNAL OF NEUROCHEMISTRY, Issue 6 2006Jennifer Q. Kwong Abstract In the past decade, the genetic causes underlying familial forms of many neurodegenerative disorders, such as Huntington's disease, Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, Friedreich ataxia, hereditary spastic paraplegia, dominant optic atrophy, Charcot-Marie-Tooth type 2A, neuropathy ataxia and retinitis pigmentosa, and Leber's hereditary optic atrophy have been elucidated. However, the common pathogenic mechanisms of neuronal death are still largely unknown. Recently, mitochondrial dysfunction has emerged as a potential ,lowest common denominator' linking these disorders. In this review, we discuss the body of evidence supporting the role of mitochondria in the pathogenesis of hereditary neurodegenerative diseases. We summarize the principal features of genetic diseases caused by abnormalities of mitochondrial proteins encoded by the mitochondrial or the nuclear genomes. We then address genetic diseases where mutant proteins are localized in multiple cell compartments, including mitochondria and where mitochondrial defects are likely to be directly caused by the mutant proteins. Finally, we describe examples of neurodegenerative disorders where mitochondrial dysfunction may be ,secondary' and probably concomitant with degenerative events in other cell organelles, but may still play an important role in the neuronal decay. Understanding the contribution of mitochondrial dysfunction to neurodegeneration and its pathophysiological basis will significantly impact our ability to develop more effective therapies for neurodegenerative diseases. [source] PURIFICATION AND CHARACTERIZATION OF A LECTIN, BRYOHEALIN, INVOLVED IN THE PROTOPLAST FORMATION OF A MARINE GREEN ALGA BRYOPSIS PLUMOSA (CHLOROPHYTA) ,JOURNAL OF PHYCOLOGY, Issue 1 2006Gwang Hoon Kim When the coenocytic green alga Bryopsis plumosa (Huds.) Ag. was cut open and the cell contents were expelled, the cell organelles agglutinated rapidly in seawater to form protoplasts. Aggregation of cell organelles in seawater was mediated by a lectin,carbohydrate complementary system. Two sugars, N -acetyl- d -glucosamine and N -acetyl- d -galactosamine inhibited aggregation of cell organelles. The presence of these sugars on the surface of chloroplasts was verified with their complementary fluorescein isothiacyanate-labeled lectins. An agglutination assay using human erythrocytes showed the presence of lectins specific for N -acetyl- d -galactosamine and N -acetyl- d -glucosamine in the crude extract. One-step column purification using N -acetyl- d -glucosamine-agarose affinity chromatography yielded a homogeneous protein. The protein agglutinated the cell organelles of B. plumosa, and its agglutinating activity was inhibited by the above sugars. Sodium dodecyl sulfate polyacrylamide gel electrophoresis results showed that this protein might be composed of two identical subunits cross-linked by two disulfide bridges. Enzyme and chemical deglycosylation experiments showed that this protein is deficient in glycosylation. The molecular weight was determined as 53.8 kDa by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The N-terminal 15 amino acid sequence of the lectin was Ser,Asp,Leu,Pro,Thr,X,Asp,Phe,Phe,His,Ile,Pro,Glu,Arg,Tyr, and showed no sequence homology to those of other reported proteins. These results suggest that this lectin belongs to a new class of lectins. We named this novel lectin from B. plumosa"bryohealin." [source] A review of morphological techniques for detection of peroxisomal (and mitochondrial) proteins and their corresponding mRNAs during ontogenesis in mice: Application to the PEX5-knockout mouse with Zellweger syndromeMICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2003Eveline Baumgart Abstract In the era of application of molecular biological gene-targeting technology for the generation of knockout mouse models to study human genetic diseases, the availability of highly sensitive and reliable methods for the morphological characterization of the specific phenotypes of these mice is of great importance. In the first part of this report, the role of morphological techniques for studying the biology and pathology of peroxisomes is reviewed, and the techniques established in our laboratories for the localization of peroxisomal proteins and corresponding mRNAs in fetal and newborn mice are presented and discussed in the context of the international literature. In the second part, the literature on the ontogenetic development of the peroxisomal compartment in mice, with special emphasis on liver and intestine is reviewed and compared with our own data reported recently. In addition, some recent data on the pathological alterations in the liver of the PEX5,/, mouse with a peroxisomal biogenesis defect are briefly discussed. Finally, the methods developed during these studies for the localization of mitochondrial proteins (respiratory chain complexes and MnSOD) are presented and their advantages and pitfalls discussed. With the help of these techniques, it is now possible to identify and distinguish unequivocally peroxisomes from mitochondria, two classes of cell organelles giving by light microscopy a punctate staining pattern in microscopical immunohistochemical preparations of paraffin-embedded mouse tissues. Microsc. Res. Tech. 61:121,138, 2003. © 2003 Wiley-Liss, Inc. [source] Inhibitory effects of furanone metabolites of a rhizobacterium, Pseudomonas jessenii, on phytopathogenic Aphanomyces cochlioides and Pythium aphanidermatumPLANT PATHOLOGY, Issue 1 2010A. Deora An antagonistic rhizobacterium, Pseudomonas jessenii EC-S101, isolated from the rhizosphere of spinach, produces two related secondary metabolites, 3-[(1R)-hydroxyoctyl]-5-methylene-2(5H)-furanone (4,5-didehydroacaterin) (1) and 3-[(1R)-hydroxyhexyl]-5-methylene-2(5H)-furanone (2). This study demonstrated their in vitro inhibitory effects, in particular those of (1), against Aphanomyces cochlioides AC-5 and Pythium aphanidermatum PA-5. The compounds inhibited radial growth and induced morphological abnormalities characterized by hyperbranching and periodic swelling in AC-5 and PA-5 hyphae, respectively. Staining with rhodamine-phalloidin, which binds to plasma-membrane-associated filamentous-actin (F-actin), revealed that tip-specific actin filaments were remodelled into a plaque-like form at an early stage of encounter (up to 24 h) with (1) or (2), whereas at later stages of encounter (48 h), the plaques were eliminated, reflecting the disorganization of actin arrays in the morphologically abnormal AC-5 and PA-5 hyphae. A similar response of actin disorganization was observed in AC-5 and PA-5 hyphae upon treatment with latrunculin B (3), an actin-assembly inhibitor produced by a sea sponge. It is suggested that (1) and (2) caused actin disorganization and their inhibitory activities were comparable to that of (3). Further ultrastructural observations substantiated abnormal functioning and delocalization of F-actin-linked cell organelles. [source] Morphology of Testes from Transgenic Rabbits: Histological and Ultrastructural AspectsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2010P. Chrenek Summary The aim of this study was to compare morphological characteristics of testes from transgenic (the WAP-hFVIII gene) and non-transgenic rabbits with emphasis on the histological and ultrastructural aspects. Samples of testes from both groups were fixed and embedded into Durcupan ACM for transmission electron microscopy. For histological analysis, semi-thin toluidine blue-stained sections were evaluated under a Jenaval light microscope. Male fertility was tested based on egg fecundity and blastocyst yield; transgene transmission was proved using PCR assay. Spermatogenesis in rabbit testes had not been destroyed both in transgenic and non-transgenic rabbits. No significant differences were found in the occurrence of individual cell organelles of the Sertoli cells in transgenic and non-transgenic rabbits. The ultrastructure of Leydig cells in testes of transgenic and non-transgenic rabbits was rather similar. No differences in the occurrence of individual organelles of Leydig cells between transgenic and non-transgenic males were found. These results were in concert with fertilizing capacity of transgenic spermatozoa. The presented status of organelles in this study indicates functional activity of the analysed cells. [source] Regional Analysis of the Ependyma of the Third Ventricle of Rat by Light and Electron MicroscopyANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2008T. C. Mathew Summary Ependymal lining of cerebral ventricles lies at the interface between the ventricular cavities and the brain parenchyma. Ependymal cells are involved in various functions within the brain and play a major role in the production of the chemical principals of the cerebrospinal fluid. Histological studies on the regional variation of the third ventricular ependyma and the subependyma of adult rats were carried out by light and electron microscopic methods. For light microscopic analysis, methacrylate sections were used. In addition to the routine haematoxylin and eosin (H and E) staining for histological studies, the sections were stained with toluidine blue, cresyl violet and periodic acid Schiff's reagent (PAS). A regional analysis of the ependyma of the third ventricle showed that in most regions the ependyma was monolayered. The sidewalls and floor of the ventral portion of the third ventricle showed a multilayered ependyma. For descriptive purposes at the light microscopic level, the ependymal cells were classified, based on the cell shape (flat, cuboidal or columnar), presence or absence of cilia and the number of cytoplasmic granules present in the cells. Studies of transmission electron microscope have shown that these granules represent the cell organelles of the ependyma. The subependyma also showed a regional morphological variation, and, in most instances, contained glial and neuronal elements. In regions of specific brain nuclei, neurons were the major cell type of the subependyma. PAS staining did not show any positive granules in the ependymal cytosol. Characteristic supraependymal elements were present at the ependymal surface of the third ventricle. [source] Synthetic cells and organelles: compartmentalization strategiesBIOESSAYS, Issue 12 2009Renée Roodbeen Abstract The recent development of RNA replicating protocells and capsules that enclose complex biosynthetic cascade reactions are encouraging signs that we are gradually getting better at mastering the complexity of biological systems. The road to truly cellular compartments is still very long, but concrete progress is being made. Compartmentalization is a crucial natural methodology to enable control over biological processes occurring within the living cell. In fact, compartmentalization has been considered by some theories to be instrumental in the creation of life. With the advancement of chemical biology, artificial compartments that can mimic the cell as a whole, or that can be regarded as cell organelles, have recently received much attention. The membrane between the inner and outer environment of the compartment has to meet specific requirements, such as semi-permeability, to allow communication and molecular transport over the border. The membrane can either be built from natural constituents or from synthetic polymers, introducing robustness to the capsule. [source] The Vibrio cholerae haemolysin anion channel is required for cell vacuolation and deathCELLULAR MICROBIOLOGY, Issue 7 2002Monica Moschioni Summary Several strains of Vibrio cholerae secrete a haemolytic toxin of 63 kDa, termed V. cholerae cytolysin (VCC). This toxin causes extensive vacuolation and death of cells in culture and forms an anion-selective channel in planar lipid bilayers and in cells. Here, we identify inhibitors of the VCC anion channel and show that the formation of the anion channel is necessary for the development of the vacuoles and for the cell death induced by this toxin. Using markers of cell organelles, we show that vacuoles derive from different intracellular compartments and we identify the contribution of late endosomes and of the trans -Golgi network in vacuole biogenesis. [source] | ||||||||||