Apoptosis Tournament
Two onboarding diagrams orient you in the apoptosis network. Then eight MCAT-DoK quiz rounds: cytochrome c's day job vs. its apoptosome role, t(14;18) follicular lymphoma logic, the intrinsic-pathway choreography, Bcl-2 family architecture, caspase-9 vs caspase-8, the heptameric apoptosome, apoptosis vs. necrosis morphology, and ALPS as a Fas-deficiency disease.
Where the Apoptosis fits in Programmed cell death
Apoptosis is the cell's controlled-demolition program: organized, ATP-dependent, and crucially non-inflammatory. Two molecular branches (intrinsic + extrinsic) converge on executioner caspases. Bcl-2 family proteins decide whether the mitochondrion permeabilizes. Click the highlighted Apoptosis box to enter the tournament.
Click the highlighted Apoptosis 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 apoptosis inside programmed cell death on the live Reactome map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways apoptosis figure before you start answering.
Fill in the Blank
Recall cytochrome c's release as the trigger for apoptosome formation.
Disruptor
Predict why t(14;18) Bcl-2 overexpression drives follicular lymphoma.
Sequence Ordering
Trace stress signal -> p53 -> Bax/Bak -> MOMP -> cytochrome c -> apoptosome -> caspase-9 -> caspase-3.
Match the Pairs
Pair each apoptotic protein (Bcl-2, Bax, Bid, caspase-8/9, FADD) with its precise role.
Numeric Input
Recall the heptameric (7-fold) apoptosome architecture.
Select All That Apply
Identify TRUE facts about apoptosis vs. necrosis: membrane integrity, ATP-dependence, PS externalization, DNA laddering.
Odd One Out
Distinguish cytochrome c (intrinsic) from extrinsic-pathway components Fas / FADD / caspase-8.
ALPS Disruptor
Recognize Fas mutations as the cause of autoimmune lymphoproliferative syndrome.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Apoptosis in 60 seconds
Apoptosis is controlled, organized, ATP-dependent cell death that removes cells without inflammation. Two pathways converge on executioner caspases (3, 6, 7): intrinsic (mitochondrial) and extrinsic (death-receptor).
The intrinsic path is decided at the outer mitochondrial membrane by the Bcl-2 family. Anti-apoptotic Bcl-2/Bcl-xL/Mcl-1 sequester pro-apoptotic Bax/Bak. BH3-only sensors (Bim, Bid, Puma, Bad) tip the balance and let Bax/Bak oligomerize, causing MOMP -> cytochrome c release -> apoptosome -> caspase-9 -> caspase-3.
The extrinsic path runs from death receptors (Fas, TNFR) through FADD -> pro-caspase-8 -> caspase-3. In Type II cells (e.g. hepatocytes) caspase-8 also cleaves Bid -> tBid, engaging the intrinsic loop for amplification.
Pharmacology: venetoclax is a Bcl-2 inhibitor (BH3 mimetic) used in CLL/AML. Apoptosis defects underlie autoimmunity (ALPS = Fas mutations) and cancer (t(14;18) follicular lymphoma; Bcl-2 overexpression). Knowing apoptosis vs. necrosis morphology is also high yield: apoptosis keeps the membrane intact; necrosis ruptures it and inflames the tissue.
FAQ
Why doesn't apoptosis cause inflammation?
Apoptotic cells maintain plasma membrane integrity throughout the process. Phosphatidylserine flipped to the outer leaflet is the 'eat me' signal, and macrophages engulf the apoptotic body before contents can spill. Necrosis, by contrast, ruptures the membrane and releases DAMPs that trigger inflammatory signaling.
What does the DNA 'ladder' represent?
Caspase-3 cleaves ICAD, releasing the active CAD endonuclease. CAD cuts DNA between nucleosomes (which protect ~146 bp), producing fragments in multiples of ~180 bp. Visualized on agarose gel, this gives the diagnostic 'ladder' pattern - distinct from the smear seen in necrosis.
How does venetoclax work?
Venetoclax is a BH3 mimetic that binds Bcl-2's hydrophobic groove, displacing pro-apoptotic Bim/Bax. With Bcl-2 neutralized, the cell's accumulated apoptotic priming triggers MOMP and apoptosis. CLL cells especially depend on Bcl-2 for survival and are exquisitely sensitive.
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
When the cell does divide - cyclin/CDK regulation, p53 / p21, the spindle assembly checkpoint.
Where cytochrome c does its day job - shuttling electrons between Complex III and IV.
Overview diagram: Reactome Pathway R-HSA-5357801, licensed CC BY 4.0.