Question

1. Describe the heterophilic interaction and homophilic interactions. Provide an example for each type of interaction.
2. Describe the structure and function of gap junction.
3. What molecules bind to intracellular receptors?
4. Hormone binding to G protein-coupled receptors induced the increase of CAMP. Describe the process.
5. List the molecules on the MAP kinase pathway.
6. Describe the major events during the 4 stages of mitosis.
7. Describe the major events during the 5 stages of prophase I in meiosis I.

Answer 1

1) The interaction between cells and that between cells and extracellular matrix are critical to the development and function of multicellular organisms. This allows cell to communicate with each other in order to regulate and perform set of activities. The property of cell adhesion is crucial as it keeps the cells attached together for proper communication and the cells recognises one another by this means. Cell adhesion involved two types of interactions- (a) Homophilic interactions- In this type of interactions, adhesion molecules on one cell interacts with similar molecules on the other cell. It leads to selective adhesion between the cells of the same type. A classic example of homophilic interaction is Cadherins which not only associated with selective adhesion but also forms stable junction between the cells. E-cadherins is expressed on epithelial cells that display homophilic binding that lead to the selective adhesion of epithelial cells to one another. (b) Heterophilic interaction- In this type of interaction, the adhesion molecule on one cell function as receptor that bind to different but specific molecule on the other cell. The binding of Intracellular adhesion molecules (ICAMs) to integrins is an example of heterophilic interaction. Here the adhesion molecule which is ICAMs recognize a different molecule which is integrin on the surface of other cell.

2) Gap junctions are a specialized junction between epithelial cells, found in most animal tissues and serves to connect the cytoplasm of adjoining cells to facilitate their communications. Gap junctions are composed of transmembrane proteins called connexins. They form hexagonal pores or channels through which transfer of ions, small molecules takes place. Each pore is made of 12 connexin molecules and six of it assemble to form a cylindrical structure. This assembly of connexins on the plasma membrane of one cell align with the connexins of adjacent cell forming an open channel between the two cytoplasms. Gap junctions facilitate the movement of ions, small molecules by providing open channels on the plasma membrane of two adjacent cells so that their cytoplasm remain connected. As a result, gap junctions couple both metabolic and physiological activities of the cells.

3) The intracellular receptors are present inside the target cells mostly in the nucleus. These receptors are membrane permeable to the molecules that bind to it. The molecules binding to intracellular receptors includes steroid hormones like cortisol, testosterone, estradiol, progesterone, etc, iodothyronines like Thyroid hormones (T3 and T4), fat soluble vitamins and small molecules like nitric oxide, etc.

4) Hormones binding to G protein-coupled receptors which induce the increase of cAMP acts via interaction with membrane-bond receptors or extracellular receptors. The process is as described below:

At first, the hormones bind with the G protein coupled receptors (GPCRs) which initiates the signal transduction. With the binding of hormone with GPCRs, it activates GTP binding regulatory proteins (G-proteins) which inturn interact with effector proteins. The extracellular or primary m,essenger, the hormone combines with the specific receptor on the plasma membrane which activates the G-protein. The activated G-protein carries the signal to adenylate cyclase. Following the event, the subunit activation of G-protein takes place and GTP binds and the beta-gamma subunits are dissociated from the alpha subunit. Adenylate cyclase is activated by G-alpha-GTP. The binding of hormone to the receptor a configurational change in the G-protein which induces the release of bound GDP and allows GTP to bind. The active G-alpha-GTP is inactivated when GTP is hydrolyzed to GTP by the activity of GTPase. Adenylate cyclase then converts ATP to cAMP which acts as secondary messenger and is produced in the cell in response to activation of adenylate cyclase by active G-protein and hydrolysis of phosphodiesterase take place. The level of cAMP in the cell is regulated by its rate of production by adenylate cyclase and hydrolysis of phosphodiesterase. The cellular level of cAMP is thus increased by inhibition of phosphodiesterase. The formation of cAMP activates the existing enzyme system of the cell and accelerates the biochemical reactions.