Practice a College Board-style free response question on Cell Communication & Cell Cycle. Write your response, then reveal the model answer to see exactly what earns each point.
A researcher studies cells with a mutation in the gene encoding a receptor tyrosine kinase (RTK). In normal cells, this RTK is activated only when a growth factor binds to it. In the mutant cells, the RTK is constitutively active — meaning it is always 'on,' even in the complete absence of the growth factor. The mutant cells are then compared to normal cells for several traits.
| Trait measured | Normal cells | Mutant cells |
|---|---|---|
| Cell division rate (with growth factor) | Normal | Normal |
| Cell division rate (without growth factor) | Stopped | Continues dividing |
| Time spent in G₁ | Long | Short |
| Tendency to form tumors in mice | None | High |
Normally, signal transduction requires reception (growth factor binds the RTK), transduction (the receptor activates a downstream cascade), and response (the cell divides). In the mutant cells, the RTK skips the reception step entirely — it is constitutively active and behaves as if a ligand is always bound, even though no growth factor is present. This means the transduction cascade is always being triggered, and the cell continuously receives the 'divide' signal. The response (cell division) therefore happens without needing the external signal.
A constitutively active RTK continuously signals the cell to divide. Normally, the cell would only pass the G₁ checkpoint if it received a proper growth factor signal AND if other conditions (size, nutrients, DNA integrity) were also met. With the RTK always signaling, the cell repeatedly receives a 'go' signal at G₁, allowing it to enter S phase and divide far more often than normal. Over many divisions, the cell may accumulate additional mutations (in tumor suppressors like p53, for example) that further disable the checkpoints. The data shows this: the mutant cells spend less time in G₁ and form tumors. Uncontrolled, repeated cell division is the defining feature of cancer.
The drug would likely slow or stop the uncontrolled division of the mutant cells. Blocking the kinase activity prevents the receptor from phosphorylating downstream proteins, which means the transduction cascade is interrupted. Without the cascade, the cell no longer receives a continuous 'divide' signal, and division should slow to normal rates (or stop entirely if no other growth signals are present). The mutant cells might also become more sensitive to apoptosis, since they have likely accumulated DNA damage from rapid divisions that normal cells would not have allowed. This is the basic strategy behind many real cancer therapies — drugs that target specific kinases activated in cancer cells.