Membrane budding in cells

Membrane Budding in Cells Membrane budding in cells Budding is an asexual reproduction, in which new off springs form from the buds of organism. The buds grow by means of cell division. The newly formed organisms stick to their parents until the moment when they mature. Membrane budding is also vesicle budding or vesicle formation. The process involves evagination of a membrane to form a vesicle. Vesicles are minute membrane enclosed sacs, which are responsible for transportation of cargo inside a cell. Vesicle budding is responsible for membrane activities such as vesicular transport and virus release. In vesicle transport, through membrane-bounded vesicle, substances move to the newly forming vesicle. All these occur during the process of budding, when they move the substances through the cell (Hurley, Boura, Carlson and Rozycki, 2010). Eukaryotic cells consist of organelles and cytoskeletons. Cytoskeletons are cellular structures in the form of a skeleton that determine the shape of a cell. Organelles refer to specialized internal structures of a cell that carry out an action. The nucleus in the cell’s surrounding, is a double membrane with pores, which facilitates movement of materials in and out of the cell. Eukaryotic cells undergo the process of mitosis where they split into two daughter cells (Bryne & Roberts, 2009). The eukaryotic cells have a structure that separates its internal organelles, in the cytoplasm. The molecules production occurs inside one organelle of a cell, but eventually released outside the cell. In the cells, vesicular transport accomplishes communication within the cell, between the internal compartments. In the beginning of the process, sorting begins with lipids and proteins. After which, the molecules include them into the waiting transport carriers. In a eukaryotic cell, budding occurs in several events. The donor membrane initiates budding of a membrane vesicle. The waiting transport carriers, transports it for fusion, with the compatible acceptor membrane. It is through the process of membrane budding that virus escapes from their host cells and infect others (Bryne & Roberts, 2009). Coated vesicle budding refers to the process of evaginizing the endoplasmic reticulum membrane to form a COPII-coated vesicle. There are two types of coated vesicle budding these are clathrin and, COP II and I. The mechanisms in clathrin involve the coating of the vesicles with clathrin to form membrane free baskets like structure. In fact, the clathrin solely relies on the adaptors for its functioning. This is because clathrin is unable to bind with both the cargo and the membrane. The adaptor protein complex, AP-2, works at the plasma of mediated-clathrin endocytosis (Hurley, Boura, Carlson and Rozycki, 2010). As a result, the protein complex, forms different types of lattices that adapt to different cargoes (Wenk & Paolo, 2012). This is a fact provided by the flexible nature of its monomers. Though clathrin, cargo adaptors and Pl (4, 5) P2 are essential in membrane curving, they cannot do this on their own. The endocytic factor in clathrin enables it to attain a positive curvature. The COP II complex coats the vesicles in COP II and I. The coated vesicles that take the shape of a basket have no membrane (Hurley, Boura, Carlson and Rozycki, 2010). During the process, COP I- coated vesicles facilitate transportation from the Golgi to the ER. The COP II monomers are flexible thus; the lattices formed are expandable and can increase, therefore, in size, to hold a large capacity of cargoes. Unlike clathrin, there is no use of adaptors instead; it uses a membrane, which consists of synthetic unsaturated phospholipids in the budding process. COP II and I are purely protein-directed membrane budding (Hurley, Boura, Carlson and Rozycki, 2010). In the formation of viruses, membrane budding is important. A number of the viruses seek the help of the Endosomal Sorting Complexes Required for Transport (ESCRT) machinery in the host cell. This machinery consists of a cytosomic protein, which includes ESCRT-0, ESCRT-II, ESCRT-III, and I. These proteins, in addition to other proteins, in the cell help to allow membrane budding away from the cytoplasm (Hurley, Boura, Carlson and Rozycki, 2010). This is because ESCRT machinery drives away from the cytosol, preventing it self from any consumption by the bud. The major functions of the ECSRT machinery, are in multivesicular body biogenesis, viral budding, and cellular abscission. Multivesicular body biogenesis refers to the process in which, proteins rich in ubiquitin, enter the endosomes, through the formation of vesicles. During this process, cells destroy the damaged proteins, thus preventing protein build up, which causes neurodegenerative diseases. On the other hand, Cellular abscission refers to the processing of cleaving a membrane that connects two daughter cells. Without cleaving the membrane, budding could result in the generation of abnormal cells that contain twice amount of DNA in them. In viral budding, the ESCRT machinery assists in the release of viruses from the cells (Wenk & Paolo, 2012). ESCRT-recruiting motifs, the late domains, have a function of enabling release and assembly of virus at the late stage. The late domain presence is in viruses such as the HIV-1 (Hurley, Boura, Carlson and Rozycki, 2010). In the absence of proteins, lipids phase separation drives budding in membranes of synthetic models on a micron scale. They enable the membrane bilayers to exist as a liquid or solid phase, depending on the temperature and the composition. Mostly, the bilayers exist as liquid phases, which divided into liquid disordered and liquid ordered phases, which can exist in mixed composition membranes. Lipids in budding sites of HIV-1 are important in forming and release of HIV-1 particles (Hurley, Boura, Carlson and Rozycki, 2010). The protein-lipid interactions help the HIV-1 in targeting its assembly in the plasma membrane for it to fuse with it, leading to release of virion. In clathrin-coated vesicle budding, the lipid PI (4, 5) P2 aids in recruiting AP-2 adaptor in the budding site. In COP II, lipids bond with the cargo to form outer cage and support budding. Despite the ability of HIV-1 to form buds, it needs the help of ESCRT, to release the buds from the host. That is HIV-1 virus is dependent on ESCRT, and interference in the ESCRT reduces the release of the HIV-1 virus (Bryne & Roberts, 2009). In conclusion, membrane budding is majorly a protein and lipid-based process. This process is important for viral reproduction. Apart from reproduction, the process is essential in transportation within the cell. Through further research in membrane budding, it will help find an amicable solution in the stopping of dangerous human pathogens such as HIV and influenza. References Byrne, H. J., Roberts, L. J. (2009). From Molecules to Networks: An Introduction to Cellular and Molecular Neuroscience. New York: Academic Press. Hurley, H. J., Boura, E., Carlson, L., Rozycki, B. (2010). Membrane Budding. Bethesda: Academic Press. Wenk, R. M., Paolo, G. D. (2012). Methods in Cell Biology: Lipids. New York: Academic Press.