Cell Cycle & Mitosis Tournament
Two onboarding diagrams orient you in the cell-cycle architecture. Then eight MCAT-DoK quiz rounds: Rb-E2F at the G1/S restriction point, paclitaxel + the spindle assembly checkpoint, the canonical M-phase choreography, cyclin/CDK pairings, chromatid arithmetic across S phase, APC/C-driven anaphase, and Li-Fraumeni syndrome.
Where the M phase fits in Cell cycle - high-level overview
The cell cycle is the four-phase decision engine that turns one cell into two. G1 -> S -> G2 -> M, gated by checkpoints that protect genomic integrity. Mitosis is the visible part; cyclin-CDK chemistry runs the show beneath. Click the highlighted M phase box to enter the tournament.
Click the highlighted M phase box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor mitosis inside the broader cell cycle on the live Reactome overview map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways cell-cycle figure before you start answering.
Fill in the Blank
Recall Rb at the G1/S restriction point: hypophosphorylated = ON (E2F sequestered).
Disruptor
Predict why paclitaxel arrests cells at metaphase via the spindle assembly checkpoint.
Sequence Ordering
Order prophase -> prometaphase -> metaphase -> anaphase -> telophase -> cytokinesis.
Match the Pairs
Pair each cyclin-CDK or regulator (D-CDK4/6, E-CDK2, A-CDK2, B-CDK1, p53, p21) with its specific phase.
Numeric Input
Count chromatids in a 2N=46 cell after S phase but before anaphase (= 92).
Select All That Apply
Identify TRUE facts about cyclin oscillation, G0 reversibility, p53 sensing, and APC/C ubiquitin ligase.
Odd One Out
Distinguish S phase (interphase) from M-phase subphases (prometaphase, anaphase, telophase).
Li-Fraumeni Disruptor
Recognize TP53 germline loss as the prototype DNA-damage-response failure that accelerates cancer.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Cell cycle in 60 seconds
The cell cycle is G1 -> S -> G2 -> M, with most cells spending the bulk of their time in G1 (or the quiescent G0 off-ramp). Each transition is gated by a cyclin-CDK pair, with checkpoints that pause the cycle if conditions aren't right.
The G1/S restriction point is the master go/no-go: cyclin D-CDK4/6 phosphorylates Rb, releasing E2F to drive S-phase gene transcription. Loss of Rb (retinoblastoma, many cancers) or constitutive cyclin D activity bypasses this checkpoint - one of the most common oncogenic events in human tumors.
Mitosis itself: prophase, prometaphase, metaphase, anaphase, telophase, then cytokinesis. The spindle assembly checkpoint (Mad2/BubR1) blocks anaphase until every kinetochore is bi-oriented. APC/C ubiquitinates securin and cyclin B to trigger sister-chromatid separation and mitotic exit.
Pharmacology: paclitaxel + docetaxel stabilize microtubules; vincristine + vinblastine destabilize them. Both jam the spindle-assembly checkpoint. p53 is the canonical DNA-damage sensor; loss (Li-Fraumeni, ~50% of all cancers) lets damaged cells continue dividing. PARP inhibitors exploit BRCA + p53-deficient tumors through synthetic lethality.
FAQ
Why is the G1/S transition called the 'restriction point'?
Past this point, the cell is committed to completing the cycle even if growth-factor signaling is removed. Before it, the cell can drop into G0 / quiescence. It is the major decision node where mitogen signaling, nutrient status, and DNA integrity all converge.
How does p53 trigger cell-cycle arrest?
Activated p53 transactivates p21 (CDKN1A), a universal CDK inhibitor that binds and inactivates G1/S and S-phase cyclin-CDK pairs. p53 also induces GADD45 (DNA repair) and BAX (apoptosis if damage is unrepairable). It is the cell's tripartite damage response.
Why does paclitaxel paradoxically work by stabilizing microtubules?
Microtubule turnover is required for orderly chromosome attachment + bi-orientation. Locked, hyperstable microtubules cannot achieve correct tension on every kinetochore, so the spindle assembly checkpoint stays active and the cell is held in mitosis. Sustained mitotic arrest -> apoptosis.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
What actually happens during S phase: helicase, polymerase, leading/lagging strands, Okazaki fragments.
When the cell decides not to divide - the intrinsic and extrinsic pathways that rebut mitosis.
Overview diagram: Reactome Pathway R-HSA-69278, licensed CC BY 4.0.