Academic Integrity: tutoring, explanations, and feedback — we don’t complete graded work or submit on a student’s behalf.

1-In normal cells an RTK receptor that binds to epidermal growth factor is prese

ID: 8955 • Letter: 1

Question

1-In normal cells an RTK receptor that binds to epidermal growth factor is present. When EGF is present in the extracellular space it binds to the receptor and initiates an RTK signal transduction cascade that ultimately tells the cell to undergo mitosis. Describe what would happen to cell division if a cell begins to express both the natural EGF receptor and a mutated version that is capable of binding to EGF. While both receptors can bind to EGF the mutated version cannot initiate receptor dimerization and autophosphorylation

Explanation / Answer

Hello!

Basically, this question is setting up the following scenario inside of a cell. You have a receptor (EGF receptor) which lures EGF out of the extracellular space. When EGF binds to the receptor, a series of reactions occurs which ultimately causes the cell to divide (undergo mitosis).

Now, suppose you have another cell. This cell has two versions of the EGF receptor: a "natural" one (which functions as described above) and a "mutant" version which binds EGF but doesn't do anything afterwards.

What ends up happening in this second cell is that EGF has a chance to bind to the "natural" receptor or to the "mutant" receptor. If it binds to the natural receptor, the cell will divide as its intended and continue on happily. If the EGF binds to the mutant receptor, the cell will fail to divide and eventually become old and die (like old skin cells).

In a healthy cell, the "natural" receptor is expressed. This means that when DNA translation took place, the "correct" version of the receptor was correctly assembled and integrated into the cell. It functions as intended.

In a diseased cell, the "mutant" receptor is expressed. This means that when DNA translation took place, the blueprint for the receptor was mis-coded and full of mistakes. This caused the cell to assemble a "mutant" or "bad" receptor which does not function as intended.

This is a very common problem we see in cancer cells (particularly those with EGF receptors).  On a side note, it's important to realize that "mutant" does not always mean "diseased." In some cases, cancer treatment is aimed at creating a "mutant" which suppresses cancer cell growth (inhibits mitosis).  That would be a situation where a "mutant" would be a good thing!

 

Hope this helps!