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Cell Biology for Bioprocessing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
Microtubules are hollow tubes formed by assembling 13 threads of α- and β-tubulins (called protofilaments) together (Figure 2.15 and Figure 2.16, Panel 2.28). Like actin filaments, the head-to-tail assembly of the monomers renders a microtubule directional, giving rise to a “+” and a “−” end. The two ends of the microtubules can extend or shrink quickly by assembling or disassembling reactions. The negative ends of many microtubules converge in an area called a microtubule organizing center (MTOC). The largest MTOC is the centrosome, from which a large number of microtubules extend their “+” ends outward. Many auxiliary proteins bind to or interact with microtubules and tubulins. A number of microtubule-associate proteins (MAPs) stabilize microtubules or facilitate the interactions of microtubules to cell components, such as binding to the cell membrane. Other auxiliary proteins promote disassembly, nucleation, bundling, or cross-linking. Microtubules are thus major structural components that affect cell shape, both statically and dynamically.
Dynein in Endosome and Phagosome Maturation
Published in Keiko Hirose, Handbook of Dynein, 2019
Ashim Rai, Divya Pathak, Roop Mallik
Endosomes/phagosomes are transported centripetally along microtubules during maturation [30, 39]. In most eukaryotic cells, microtubules are arranged in a polarized manner with plus ends located at the cell periphery near the plasma membrane and minus ends located at the microtubule organizing center (MTOC) present near the nucleus. Cytoplasmic dynein (hereafter referred to as dynein) is the primary microtubule-based motor for minus-directed (i.e., retrograde or centripetal) transport of endosomes/phagosomes [1]. Research over the past few decades has led to a deeper understanding of dynein structure, biophysical properties and regulation (see other chapters in this volume). The repertoire of dynein-driven cellular cargoes and the mode of dynein recruitment to them is impressive. We will dwell on these aspects briefly before focusing on dynein function in endosome and phagosome transport and maturation. We will also highlight how intracellular pathogens hijack and inhibit dynein-driven endosome and phagosome transport to survive inside cells [33]. To end, we will emphasize on the crucial role played by lipids in regulation of dynein driven endosome/phagosome transport.
Nanomaterials against pathogenic viruses: greener and sustainable approaches
Published in Inorganic and Nano-Metal Chemistry, 2020
Ghazaleh Jamalipour Soufi, Siavash Iravani
Generally, important antiviral approach is to block the receptor of the host cell membrane by applying recombinant viral proteins or virus antiserum. Additionally, in order to interference with the ligand-receptor binding, disrupting the structure of the virus envelope can be considered for combating viral infections. Carbon quantum dots with their suitable advantageous properties, such as low cytotoxicity, small size, low-cost and simple preparation and modification, showed high antiviral and antibacterial activities.[18,48] High-photoluminescence quantum dots for labeling viruses are very promising for understating the viral infection mechanistic aspects;[49] a critical challenge is labeling internal viral components efficiently with no viral envelope/capsid modifications. Importantly, an innovative strategy was applied for the clustered regularly interspaced short palindromic repeats imaging system to label the nucleic acids of Pseudorabies virus (PRV) with quantum dots. Consequently, quantum dots were conjugated to viral nucleic acids with the assistance of nuclease-deactivated Cas9/gRNA complexes in the nuclei of living cells and then packaged into PRV during virion assembly.[49] The cytoplasmic transport along microtubules, PRV-quantum dot adsorption, nuclear entry in real time in both Vero and HeLa cells were monitored.[49] Additionally, the influence of quantum dot labeling on virus activity, cell viability and cytokine secretion were evaluated after host cells were infected by quantum dot-labeled H9N2 and unlabeled H9N2.[50] It was reported that in the procedure of quantum dot labeling, biotin modification (<1 mg/mL) had no noticeable influence on virus activity. Though, follow-up quantum dot labeling improved the virus toxicity toward host cells and produced remarkable level of cytokine secretion; it was revealed that quantum dot-labeling was not appropriate for long time tracing of viruses.[50] For evaluation of the infection mechanism of PEDV, which causes porcine epidemic diarrhea, a highly contagious enteric disease, quantum dot labeled approach was applied to hold intact infectivity of the labeled viruses to the largest extent, with the single particle tracking method to dynamically and globally visualize the transport behaviors of PEDVs in live Vero cells (Figure 4).[51] It was revealed that PEDVs kept limited motion mode with a relatively stable speed in the cell membrane region; while accomplished a slow-fast-slow velocity pattern with various motion modes in the cell cytoplasm region and near the microtubule organizing center region.[51] Further, the return movements of small amount of PEDVs have been detected in the live cells. By applying quantum dots labeling, it can be understand the mechanistic aspects of viral movement (like PEDV in the live cells), and suitable informative information can be obtained for further evaluation and academic researches on the viral infection mechanisms.[51]