2 edition of Influence of anti-microtubule agents on cell morphogensis in Trypanosoma Brucei. found in the catalog.
Influence of anti-microtubule agents on cell morphogensis in Trypanosoma Brucei.
Thesis (M.Sc.), - University of Manchester, School of Biological Sciences.
|Contributions||University of Manchester. School of Biological Sciences.|
|The Physical Object|
|Number of Pages||207|
The main cytoplasmic elements which seem important in scale morphogenesis, on the basis of frequency, orientation and grouping, are A fibrils and microtubules. Full Text The Full Text of this article is available as a PDF (M). It has long been known that the pathogens causing sleeping sickness evade the immune system by exchanging their surface proteins. But now scientists at the German Cancer Research Center have found an additional parasite strategy to escape the immune system: They confuse the defense system with sugar. The sugar chains on the coat protein prevent the binding of protective antibodies and thus. Microtubules are important cellular targets for anticancer therapy because of their key role in mitosis. Microtubule inhibitors (MTI) such as taxanes, vinca alkaloids, and epothilones stabilize or destabilize microtubules, thereby suppressing microtubule dynamics required for proper mitotic function, effectively blocking cell cycle progression and resulting in apoptosis. Colchicine treatment inhibits the ‘semi‐lobed’ morphogenesis of epidermal cells and mesophyll cells surrounding the endodermis and the concomitant intercellular space opening. These observations reveal that the primary event of ‘semi‐lobed’ cell morphogenesis is the organization of two different patterns of the cortical microtubule.
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Trypanosoma brucei, the focus of this study, is the causal agent of human African sleeping sickness and livestock trypanosomiasis; it is transmitted between mammals by tsetse Influence of anti-microtubule agents on cell morphogensis in Trypanosoma Brucei.
book and seven morphologically distinct forms of the parasite are currently recognised (Sharma et al. ; Van Den Abbeele et al. ; Vickerman). Of these Cited by: Basal body movements orchestrate membrane organelle division and cell morphogenesis in Trypanosoma brucei.
J Cell Sci– Crossref, Medline, Google Scholar; LaCount DJ, Barrett B, Donelson JE (). Trypanosoma brucei FLA1 is required for flagellum attachment and cytokinesis. J Biol Chem– Crossref, Medline Cited by: Abstract. In the unicellular parasite Trypanosoma brucei, the causative agent of human African sleeping sickness, complex swimming behavior is driven by a flagellum laterally attached to the long and slender cell body.
Using microfluidic assays, we demonstrated that T. brucei can penetrate through an orifice smaller than its maximum diameter. Efficient motility and penetration depend on Cited by: Importance: Trypanosoma brucei is a single-celled parasite that is transmitted between humans and other animals by the tsetse fly.
brucei is endemic in sub-Saharan Africa, where over 70 million. In procyclic Trypanosoma brucei, TbCentrin2 and TbCentrin4 have distinct effects on cell division but both localize to the basal bodies that seed the flagellum, and a bi-lobed structure important. Lacomble S, Vaughan S, Gadelha C, Morphew M, Shaw M, 'Basal body movements orchestrate membrane organelle division and cell morphogenesis in Trypanosoma brucei' Journal of Cell Science (17) () pp ISSN: eISSN: Abstract.
The mitochondrial DNA of Trypanosoma brucei is organized in a complex structure called the kinetoplast. In this study, we define the complete kinetoplast duplication cycle in T. brucei based on. In the unicellular parasite Trypanosoma brucei, the causative agent of human African sleeping sickness, complex swimming behavior is driven by a flagellum laterally attached to the long and slender cell body.
Using microfluidic assays, we demonstrated that T. brucei can penetrate through an orifice smaller than its maximum diameter.
Efficient motility and penetration depend on active flagellar. Cell body morphogenesis of a promastigote and trypomastigote through the cell cycle. kmcb// Accessed 13 June glycoprotein in Trypanosoma brucei.
J Cell. The tubulin cofactor C domain-containing protein TbRP2 is a basal body (centriolar) protein essential for axoneme formation in the flagellate protist Trypanosoma brucei, the causal agent of. NCI's Dictionary of Cancer Terms provides easy-to-understand definitions for words and phrases related to cancer and medicine.
A mitotic inhibitor is a drug that inhibits mitosis, or cell drugs disrupt microtubules, which are structures that pull the chromosomes apart when a cell c inhibitors are used in cancer treatment, because cancer cells are able to grow and eventually spread through the body (metastasize) through continuous mitotic division.
An antimicrotubule agent is a type of drug that blocks cell growth by stopping mitosis (cell division). Antimicrotubule agents interfere with microtubules (cellular structures that help move chromosomes during mitosis).
They are used to treat cancer. This answer is based on source information from the National Cancer Institute. Sherwin T, Gull K () The cell division cycle of Trypanosoma brucei brucei: timing of event markers and cytoskeletal modulations.
Phil Trans R Soc Lond B – CrossRef Google Scholar Soares TC, De Souza W () Fixation of trypanosomatids for electron microscopy with the glutaraldehyde-tannic acid method. In contrast, they were found to react only with tubulin in Trypanosoma brucei, parasitic protozoan which are the causative agent of sleeping sickness.
By immunofluorescence microscopy, 3F3 bound only to a subpopulation of microtubules associated with the flagellum of these cells when, under the same conditions, 16D3 stained other microtubule.
The differing degrees of correlation of cell body and flagellum length of juxtaforms and liberforms (Figure 4 and and5) 5) suggest the morphogenesis of T. brucei and L. mexicana are representative of these two superclasses respectively, with lateral flagellum attachment and flagellum length mediating control of cell length in juxtaforms but not.
MCAK and anti-microtubule agents Cell Cycle ; Vol. 7 Issue 14 MCAK knockdown disrupted mitotic spindles (Fig. 2A),18,19 Prometaphase cells often had an increase in MTs that emanated toward the cell cortex and appeared to originate from the poles, a phenotype we refer to as “hairy” spindles (Fig.
2A). In addition MTs. Tetley, L., and Vickerman, K.,Differentiation in Trypanosoma brucei: Host-parasite cell junctions and their persistence during acquisition of the variable antigen coat, J.
Cell. Direct anti-proliferative effects of MBDs on endothelial cells are likely only partly responsible for their anti-vascular actions. It is not surprising that at appropriate concentrations, MBDs are cytotoxic toward endothelial cells and can inhibit their proliferation (3, 4, 9, 18, 19, 28).In fact, in some instances, endothelial cells are more sensitive to growth inhibition by MBDs than are.
Trans. Fong, D. () Effect of the anti-microtubule compound tubulozole on Leishmania proto-zoan parasites in vitro. Timing of nuclear and kinetoplast DNA replication and early morphological events in the cell cycle of Trypanosoma brucei. Cell Sci.
The cell cycle and cytoskeletal morphogenesis in. Screening for Essential Genes Involved in Mitochondrial Morphogenesis. After thawing well plates containing frozen stocks of the yeast strains, cells were transferred to yeast extract/peptone/glucose (YPD) plates without or with 10 μg/ml doxycycline using a sterile pinning tool and incubated at 30°C over night.
The dependency relationships between cell cycle events, basal body/flagellum-linked structures and morphogenesis in T. brucei were established via the use of DNA synthesis inhibitors, anti-microtubule agents and the production of mutants defective in flagellum assembly [17–21].
STEM CELLS, ISSN06/, Vol Issue 6, pp. - Full Text Rab11 mediates selective recycling and endocytic trafficking in Trypanosoma brucei.
by Umaer, Khan and Bush, Peter J and Bangs, Full Text Eph/ephrin signaling in morphogenesis, neural development and plasticity. by Klein, Rüdiger. Current Opinion in Cell. In a study discussed in the chapter, four Zebu cattle were inoculated intravenously with 10 mouse ID 63 of a recent isolate (EATRO-3) of the Trypanosoma brucei subgroup, preserved in lymph tubes at approximately −80°C.
Three serological tests were used in the investigation, an agglutination test, an agar gel double diffusion test, and a. Sub-species of Trypanosoma brucei are the causal agents of human African sleeping sickness and Nagana in domesticated livestock.
These pathogens have developed an organelle-like compartment called the flagellar pocket (FP). The FP carries out endo- and exocytosis and is the only structure this parasite has evolved to do so. The FP is essential for parasite viability, making it an interesting.
Sleeping sickness, also known as African trypanosomiasis, is caused by the parasitic flagellate Trypanosoma brucei, which is injected into the body by the tsetse fly. The disease occurs only in the 25 sub-Saharan African countries exposed to the tsetse fly.
It can affect humans and animals, particularly cattle. Following efforts to combat the disease, the number of cases has fallen since with the host cytoskeleton during cell invasion (Morisaki et al., ; Dobrowolski and Sibley, ).
gondii is of similar size to T. cruzi and, like T. cruzi, invades most nucleated cell types in a period of less than 30 min, mak-ing it a good control organism for our investigation. We. Biol - - Biology bibliographies - in Harvard style.
Change style powered by CSL Popular AMA APA (6th edition) APA (7th edition) Chicago (17th edition, author-date) Harvard IEEE ISO MHRA (3rd edition) MLA (8th edition) OSCOLA Turabian (9th edition) Vancouver. The increasing detection of infections of Trypanosoma cruzi, the etiological agent of Chagas disease, in non-endemic regions beyond Latin America has risen to be a major public health issue.
With an impact in the millions of people, current treatments rely on antiquated drugs that produce severe side effects and are considered nearly ineffective for the chronic phase. We found that MCAK knockdown increased the morphological defects of the microtubule cytoskeleton in HeLa cells caused by anti-microtubule drugs.
Our studies support the idea that MCAK would be a good target for new chemotherapeutic development and may be particularly useful in combination therapies with currently available anti-microtubule agents.
Treatment of animal African trypanosomiasis (AAT) requires urgent need for safe, potent and affordable drugs and this has necessitated this study. We investigated the trypanocidal activities and mode of action of selected 3-aminosteroids against Trypanosoma brucei brucei.
The in vitro activity of selected compounds of this series against T. congolense (Savannah-type, IL), T.
brucei. Athough the literature contains a scattering of reports of MAP2-like proteins in invertebrates (e.g. Refs. 42, 54) that are recognized by anti-mammalian MAP2, there is a lesson to be learned from studies of MAPs in the protozoan Trypanosoma brucei.
Microtubule-interacting drugs are important agents in cancer chemotherapy. Some of these drugs alter microtubule dynamics and engage the cell cycle surveillance mechanisms to arrest cell division in mitosis.
Many cancer cells possess genetic lesions in components of this pathway and thus fail to arrest in mitosis. Therefore, by targeting the spindle microtubules, chemotherapeutic agents can. Treatment of filamentous fungal infections relies on a limited repertoire of antifungal agents.
Compounds possessing novel modes of action are urgently required. N-myristoylation is a ubiquitous modification of eukaryotic proteins. The enzyme N-myristoyltransferase (NMT) has been considered a potential therapeutic target in protozoa and yeasts. Here, we show that the filamentous fungal.
This important volume offers an integrated view of the principal aspects of immune response to all types of infectious agents, with an emphasis on the immune system as a host defense system.
The various infectious agents and diseases are integrated under general topics rather than treated in separate chapters. The book illustrates how the dialogue between different types of pathogens and the. J Cell Biol. Jan; 72 (1)– [PMC free article] Eichhorn JH, Peterkofsky B.
Local anesthetic-induced inhibition of collagen secretion in cultured cells under conditions where microtubules are not depolymerized by these agents.
J Cell Biol. Apr; 81 (1)– [PMC free article] Flaumenhaft E, Bose S, Crespi HL, Katz JJ. DNA methylation (m5C) in both bloodstream form as well as the procyclic form of Trypanosoma brucei was identified by analysis using liquid chromatography and mass spectrometry.
Also DNA from Trypanosoma cruzi was found to harbor the same mark of DNA modification, m5C (albeit at a completely different restriction site unlike the canonical. Microtubule-interacting drugs for cancer treatment Paula M. Checchi1,3, James H. Nettles2,4, Jun Zhou1,3, James P.
Snyder2 and Harish C. Joshi1 1Department of Cell Biology, Emory University School of Medicine, Atlanta, GAUSA 2Department of Chemistry, Emory University, Atlanta, GAUSA 3Program in Biochemistry, Cell and Developmental Biology, Emory University, Atlanta, GA.
Microtubules and microfilaments play important roles in cell morphogenesis. The picture emerging from drug studies and molecular-genetic analyses of mutant higher plants defective in cell morphogenesis shows that the roles played by them remain the same in both tip-growing and diffuse-growing cells.
Microtubules are important for establishing and maintaining growth polarity whereas actin. Glycosylphosphatidylinositol (GPI) anchoring provides an alternative to transmembrane domains for anchoring proteins to the cell surface in eukaryotes.
GPI anchors are synthesized in the endoplasmic reticulum via the sequential addition of monosaccharides, fatty acids, and phosphoethanolamines to phosphatidylinositol.
Deficiencies in GPI biosynthesis lead to embryonic lethality in animals and. To explore the molecular alterations underlying acquired resistance to anti-microtubule agents, we performed a gene expression array analysis comparing HCCER cells with parental HCC cells.
Expression of CDH1 in HCCER cells was significantly decreased compared with HCC cells, confirming the previous report (Table 3) [ 10 ]. The trypanosome cell surface is covered by a dense coat made up of very many copies of a single protein, called variable surface glycoprotein (VSG).
A glycoprotein is a protein with carbohydrate (sugar) groups attached to one or more amino acid sidechains; the word "variable" is used because there are about variants of this protein.Abstract. Trypanosoma cruzi has a complex life cycle which involves infection of vertebrate hosts and transmission by insect vectors.T.
cruzi progresses through a number of quite different sites in its host and vector and the differentiation of the parasite through several distinct stages reflects its adaptation to the cyclical variation in its environment.