Regulation of Cell Cycle

CDK stays at 59-61 units throughout; cyclin climbs from 8 to 90 units over about 20 hours, then falls to 15 within an hour, twice.

• Correct: CDK protein stays level, while cyclin builds slowly and drops sharply at each mitosis.: Only cyclin cycles; CDK protein is flat.
• CDK protein and cyclin rise and fall together, both peaking at each mitosis.: CDK protein does not change.
• Cyclin stays level, while CDK protein builds up slowly over time and drops at each mitosis.: This reverses the two proteins.
• Cyclin and cyclin-CDK activity both stay low except during S phase.: Both peak at mitosis, around 20 and 42 hours, not in S phase.

CDK never changes, so it cannot explain when activity rises; activity rises and falls with cyclin.

• Correct: The timing of cyclin-CDK activity is set by the amount of cyclin, not the amount of CDK.: Activity tracks cyclin; CDK is constant.
• The timing of cyclin-CDK activity is set by the amount of CDK, not the amount of cyclin.: CDK is flat, so it cannot set the timing.
• Cyclin-CDK activity rises steadily with cyclin through interphase, matching its level at each time.: Activity stays at 6 units or less until cyclin is above about 60 units, then jumps: it does not rise steadily with cyclin.
• Cyclin-CDK activity is highest in G1, when the cell decides whether to divide.: Activity of this mitotic cyclin-CDK peaks at mitosis, not in G1.

Destroying cyclin is what switches CDK off so the cell can leave mitosis. With cyclin that stays, the complex stays active and the cells remain stuck in mitosis.

• Correct: The cells enter mitosis, but cyclin-CDK activity stays high and they cannot finish dividing.: Entry needs high activity, which happens; exit needs cyclin destroyed, which cannot happen.
• The cells skip mitosis and start copying their DNA again, because cyclin is already high.: High mitotic cyclin-CDK drives mitosis, not a new round of copying.
• The cells do not enter mitosis, because a cyclin that resists destruction is unable to bind CDK.: The stem says this cyclin binds CDK normally.
• The cells divide normally, because CDK protein, which sets the timing, is not changed.: The data show the timing follows cyclin, not CDK.

Working p53 is the only difference between the lines. p53 halts the cycle at G1 (more cells in G1) and triggers apoptosis in cells it cannot save (rising apoptosis).

• Correct: Damaged DNA raises p53, which holds cells at the G1 checkpoint and triggers apoptosis if repair fails.: Both effects appear only where p53 works.
• X-rays destroy cyclins directly, so cells in line N stop wherever they are in the cycle and then they die.: Line P received the same X-rays and did not stop, so X-rays do not halt cells directly.
• p53 repairs the broken DNA itself, and cells wait in G1 until p53 has finished each repair.: p53 halts the cycle and switches on genes; it does not repair DNA itself.
• X-rays speed up S phase in line N, so more cells reach G1 sooner and wear out by apoptosis.: Cells build up in G1 because they are held there, not because they move through S faster.

Without p53, cells with damaged DNA neither stop for repair nor die; their damage is copied into daughter cells as mutations, which is how losing p53 raises cancer risk.

• Correct: They carry more mutations, because damaged DNA was copied, not repaired or removed.: Skipping the halt and apoptosis lets damage become permanent mutations.
• They carry fewer mutations, because without p53 the damaged cells die faster.: Line P shows almost no apoptosis, so damaged cells survive rather than die.
• They carry the same mutations, because both lines received the same dose of X-rays.: The dose was the same, but line N halted and removed damaged cells, so fewer mutations were passed on.
• They stop dividing within a day, because damaged DNA is impossible to copy.: Line P cells keep cycling (38-44% in G1, like unexposed cells), so damaged DNA is copied.