AcornPrep

AP Biology Unit 4: Cell Communication and Cell Cycle — Worked Examples

Constitutively Active Ras and Uncontrolled Cell Division

Hard

A somatic cell acquires a point mutation in the Ras gene that prevents the Ras protein from hydrolyzing GTP to GDP. Ras is a G protein in the MAP kinase signaling pathway that promotes cell division when activated by growth factor binding. What is the most likely consequence of this mutation?

  1. The cell will not respond to growth factors because Ras cannot be activated
  2. The cell will divide only when growth factor is present, but at an accelerated rate
  3. The cell will undergo continuous cell division regardless of growth factor presence ✓ Correct
  4. The cell will undergo apoptosis because the signaling pathway is disrupted
Solution

Ras is a molecular switch: active when bound to GTP and inactive when it hydrolyzes GTP to GDP. If Ras cannot hydrolyze GTP, it is permanently locked in the active (GTP-bound) state. This sends a continuous 'divide' signal through the MAP kinase cascade regardless of whether growth factor is bound to the receptor. This is an oncogenic mutation. Choice A confuses a loss-of-function mutation (cannot bind GTP) with this gain-of-function mutation (cannot release GTP). Choice B incorrectly assumes growth factor is still required — the permanently active Ras bypasses the receptor. Choice D assumes pathway disruption triggers apoptosis, but this is pathway hyperactivation, not disruption.

p53 Mutation and G1/S Checkpoint Failure

Hard

A researcher exposes two cell cultures to UV radiation, which causes thymine dimers in DNA. Culture A has normal p53 function. Culture B has a homozygous loss-of-function mutation in the TP53 gene. The researcher then monitors cell cycle progression. Which prediction is best supported by current understanding of cell cycle regulation?

  1. Culture A cells arrest in G1; Culture B cells also arrest but at the G2/M checkpoint instead
  2. Culture A cells arrest in G1 and may repair DNA or undergo apoptosis; Culture B cells proceed into S phase with damaged DNA ✓ Correct
  3. Both cultures arrest at the G1/S checkpoint because DNA damage is detected independently of p53
  4. Culture A cells repair DNA during S phase; Culture B cells undergo immediate apoptosis due to accumulated damage
Solution

p53 is the central mediator of the G1/S checkpoint. When DNA damage is detected, p53 activates transcription of p21, which inhibits cyclin-CDK complexes and arrests the cell in G1. This allows time for DNA repair; if repair fails, p53 can trigger apoptosis. Without functional p53 (Culture B), the G1/S checkpoint fails, and cells proceed into S phase and replicate damaged DNA, potentially accumulating mutations. Choice A incorrectly assumes the G2/M checkpoint fully compensates for p53 loss — while G2/M provides some backup, the primary response to UV damage is p53-mediated G1 arrest. Choice C incorrectly states the G1/S checkpoint is p53-independent. Choice D reverses the outcomes — normal cells arrest first (not repair during S), and p53-deficient cells proliferate rather than undergoing apoptosis.