Budding events

The vesicles that bud into the interior of endosomes have a topology similar to that of enveloped virus particles that bud from the plasma membrane of virus-infected cells. Moreover, recent experiments demonstrate that a common set of proteins are required for both types of membrane-budding events. In fact, the two processes so closely parallel one another in mechanistic detail as to suggest that enveloped viruses have evolved mechanisms to recruit the cellular proteins used In Inward endosomal budding for their own purposes. 

Cyster. When you are forming a new lymphatic vessel in an adult mouse or human, is it thought to be a budding event, or is it coalescence of some t)rpe of cell ... 

Biochemical characterization of clathrin-coated vesicles revealed that their major coat components are clathrin and various types of adaptor complexes. Clathrin assembles in triskelions that consist of three heavy chains of approximately 190 kDa and three light chains of 30 40 kDa. Four types of adaptor complexes have been identified to date, AP-1, AP-2, AP-3 and AP-4 (AP for adaptor protein). Whereas AP-1, AP-3 and AP-4 mediate sorting events at the TGN and/or endosomes, AP-2 is involved in endocytosis at the plasma membrane. Each adaptor complex is a hetero-tetrameric protein complex, and the term adaptin was extended to all subunits of these complexes. One complex is composed of two large adaptins (one each of y/a/S/s and [31-4, respectively, 90-130 kDa), one medium adaptin (pi -4, <50 kDa), and one small adaptin (ol-4, <20 kDa). In contrast to AP-1, AP-2 and AP-3, which interact directly with clathrin and are part of the clathrin-coated vesicles, AP-4 seems to be involved in budding of a certain type of non-clathrin-coated vesicles at the TGN. 

Vesicles lie at the heart of intracellular transport of many proteins. Recently, significant progress has been made in understanding the events involved in vesicle formation and transport. This has transpired because of the use of a number of approaches. These include establishment of cell-free systems with which to study vesicle formation. For instance, it is possible to observe, by electron microscopy, budding of vesicles from Golgi preparations incubated with cytosol and ATP. The development of genetic approaches for studying vesicles in yeast has also been crucial. The piemre is complex, with its own nomenclamre (Table 46-7), and involves a variety of cytosolic and membrane proteins, GTP, ATP, and accessory factors. 

That the initial event of taste stimulation takes place on the cell surface of the taste receptor is now universally accepted. In addition, accumulated evidence strongly suggests that taste-bud stimulation is extracellular in nature. For example, (1) the sweet-taste response is both rapid and reversible, (2) the intensely sweet proteins monellin" and thaumatin could not possibly penetrate the cell, because of their size, and (3) miraculin, the taste-modifying glycoprotein, having a molecular weight of 44,000 would also be too large to penetrate the taste cell. ... 

Taste-modality recognition is a function of the cells of the taste buds. Perception of the sensation is a result of complex processes in the brain. The biological events that are discussed are those that occur, or are suggested as occurring, in taste-receptor cells, beginning at the instant when the taste-stimulus molecule interacts with the cell, until the membrane of the receptor cell is polarized. These are peripheral events. However, our knowledge of the peripheral mechanisms in taste perception is not sufficiently complete to provide a detailed, biophysical explanation of this phenomenon. Nevertheless, several stages in this explanation have been hypothesized, and some are demonstrable. 

The vegetative cell cycle of S. cerevisiae has received extensive attention. There are many justifications for this. Firstly, the cell cycle in this organism has many convenient landmarks (Hartwell 1974, 1978 Pringle 1978) which make it very easy to identify the exact point in the cell cycle at which a cell happens to be. Examples of these landmark events include bud emergence, the size of the bud, mitosis (nuclear division takes place through the neck between the mother cell and the bud), and cell... 

Nasmyth There are many examples where this is a stochastic event. Stochastic can refer to genes flicking on and off, or it can be choosing a position on the cell and marking that point — budding in yeast is a good example of this. Also, in the lateral inhibition, it is which one of the neuroblasts will win out. Once you have established this, you have created a focus for generating asymmetry. 

After induction, two events occur condensation of the mesenchyme around the ureteric bud, and transformation of the mesenchyme into epithelium. In order for condensation into a comma-shaped mass to occur, there has to be induction of a critical mass of cells, not all of which appear to be in contact with the ureteric bud. There appears to be some short-range signalling in the mesenchyme involving the secreted glycoprotein WNT-4. Mice lacking WNT-4 fail to form pretubular aggregates (as do PAX-2 knockouts). There also appears to be migration of induced cells away from direct contact with the ureteric bud, often several cell diameters distant. This may permit uninduced cells to contact the ureteric bud. 

Figure 28-27 General features of the HIV-1 replication cycle. The early phase (upper portion of the diagram) begins with CD4 recognition and involves events up to and including integration of the proviral DNA, and the late phase includes all events from transcription of the integrated DNA to virus budding and maturation. From Turner and Summers.735...

A number of products exist that are targeted at any of the successive events implicated in the replicative cycle of HIV virus entry, viral adsorption, virus-cell fusion, reverse (RNA —> DNA) transcription, proviral DNA integration, viral (DNA —> RNA) transcription (transactivation), viral (mRNA —> protein) translation, virus release, viral assembly, budding, and maturation... 

Protein transport between intracellular compartments is mediated by a mechanism that is well-conserved among all eukaryotes, from yeast to man. The transport mechanism involves carrier vesicles that bud from one organelle and fuse selectively to another. Specialized proteins are required for vesicle transport, docking, and fusion, and they have been generically named SNAREs (an acronym for soluble N-ethylma-leimide-sensitive fusion attachment protein receptor). SNAREs have been divided into those associated with the vesicle (termed v-SNAREs), and those associated with the target (termed t-SNAREs). The key protein, which led to the discovery of SNAREs was NSF, an ATPase found ubiquitously in all cells, and involved in numerous intracellular transport events. The subsequent identification of soluble proteins stably bound to NSF, the so-called SNARE complex, led to the formulation of the SNARE hypothesis, which posits that all intracellular fusion events are mediated by SNAREs (Rothman, 2002). 

It is generally accepted that a drug initiates a chain of events which eventually leads to a specific biological effect but which does not involve the drug after it triggers the mechanism through a drug-receptor interaction. For example, sucrose tastes sweet, but the role of sucrose molecules is to stimulate the taste buds, and they do not participate in the process of sensory conduction as such. 

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