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This deck focuses on Regulation Of Cell Cycle, giving you a quick way to review the definitions, rules, and examples that matter most for AP Biology.
Study Regulation Of Cell Cycle in AP Biology with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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Which protein complex ensures proper chromosome separation?
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Cohesin complex. Holds sister chromatids together until anaphase.
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This deck focuses on Regulation Of Cell Cycle, giving you a quick way to review the definitions, rules, and examples that matter most for AP Biology.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Cohesin complex. Holds sister chromatids together until anaphase.
Answer: Cytokinesis divides cytoplasm; mitosis divides the nucleus. Two distinct processes that together complete cell division into daughter cells.
Answer: Separation of sister chromatids. Cohesin cleavage allows chromosome movement to poles.
Answer: DNA replication occurs. Chromosome duplication creates sister chromatids.
Answer: It induces p21 to inhibit CDKs and arrest the cycle (often at G1). p21 binds and inhibits CDK complexes needed for S-phase progression.
Answer: Prometaphase. Transition phase where kinetochore assembly occurs.
Answer: Chromosome mis-segregation leading to aneuploid daughter cells. Unequal chromosome distribution creates cells with abnormal chromosome numbers.
Answer: Cyclin-dependent kinases (CDKs). Phosphorylate target proteins when bound to cyclins.
Answer: Accelerated entry into S phase. Excessive cyclin E bypasses normal checkpoint control.
Answer: p53 protein. Guardian of the genome; halts cycle for DNA repair.
Answer: Telophase. Final mitotic phase reverses nuclear breakdown.
Answer: S phase. Synthesis phase duplicates chromosomes for division.
Answer: Cytokinesis. Contractile ring pinches cell membrane in two.
Answer: Failure to enter anaphase due to securin and cyclin persistence. Unable to degrade key proteins required for anaphase progression and mitotic exit.
Answer: They rise and fall due to regulated synthesis and proteasomal degradation. Periodic destruction and synthesis creates oscillating levels that drive transitions.
Answer: Crowding reduces division via cell-cell contact and signaling. Contact inhibition prevents overgrowth when cell density becomes too high.
Answer: DNA replication occurs. Chromosome duplication creates sister chromatids.
Answer: Activation of cyclin B/CDK1 complex. Active kinase triggers nuclear envelope breakdown.
Answer: They provide external signals that stimulate passage through G1. Signal adequate nutrients and conditions for cell division to proceed.
Answer: G₂/M checkpoint. Ensures cell is ready for nuclear division.
Answer: The G1 checkpoint (restriction point in animals). Prevents S-phase entry if growth conditions are inadequate or DNA is damaged.
Answer: After S phase (during G2 and early M). Sister chromatids remain attached until anaphase when cohesin is cleaved.
Answer: Separase. Protease cleaves cohesin rings holding chromatids.
Answer: The M checkpoint (spindle assembly checkpoint). Prevents chromosome mis-segregation by ensuring proper spindle attachment.
Answer: Anaphase-promoting complex (APC). Ubiquitin ligase targets cyclins for destruction.
Answer: It inhibits E2F, preventing transcription of S-phase genes. Hypophosphorylated Rb sequesters E2F; phosphorylation releases E2F to activate S-genes.
Answer: Cells must attach to a surface (ECM) to progress through the cell cycle. Prevents division of cells that have lost proper tissue contact.
Answer: Metaphase. Chromosomes align at metaphase plate before separation.
Answer: p53 protein. Activates apoptotic pathway when damage is severe.
Answer: Covalent tagging of proteins for degradation by the proteasome. Small protein tag that marks regulatory proteins for destruction by proteasome.
Answer: Regulate the progression of the cell cycle. Oscillating proteins that activate CDKs at checkpoints.
Answer: The M checkpoint (spindle assembly checkpoint). Prevents chromosome mis-segregation by ensuring proper spindle attachment.
Answer: Anchorage-independent growth. Cancer cells can divide without attachment to extracellular matrix or surfaces.
Answer: A control point that can pause progression until conditions are correct. Ensures proper order and prevents errors by monitoring completion of previous events.
Answer: G₀ phase. Quiescent state for non-dividing differentiated cells.
Answer: The G2 checkpoint. Detects incomplete DNA synthesis and halts progression until replication finishes.
Answer: They bind CDKs and activate them at specific cell-cycle stages. Cyclins provide timing and specificity by accumulating at precise cell-cycle phases.
Answer: Cytokinesis. Physical division of cytoplasm creates two cells.
Answer: The G2 checkpoint. Detects incomplete DNA synthesis and halts progression until replication finishes.
Answer: Chk1 kinase. DNA damage checkpoint kinase prevents mitotic entry.
Answer: Activation of cyclin B/CDK1 complex. Active kinase triggers nuclear envelope breakdown.
Answer: Prophase. First phase organizes chromosomes for division.
Answer: APC/C (anaphase-promoting complex/cyclosome). Ubiquitin ligase that targets securin and M-cyclins for proteasomal degradation.
Answer: Chromosome mis-segregation leading to aneuploid daughter cells. Unequal chromosome distribution creates cells with abnormal chromosome numbers.
Answer: Inhibits CDKs to regulate cell cycle entry. Phosphorylates CDK1 to keep it inactive until appropriate.
Answer: The G2 checkpoint. Prevents mitosis when DNA replication errors or damage are detected.
Answer: G2 phase. Cell synthesizes proteins required for chromosome condensation and spindle formation.
Answer: G₁ phase. Gap phase for organelle synthesis and growth.
Answer: Phosphorylation of Rb by cyclin-CDK complexes. Phosphorylated Rb releases E2F transcription factor to promote S-phase entry.
Answer: They phosphorylate target proteins to drive cell-cycle transitions. Phosphorylation activates substrates that control key transitions like S-phase entry or mitosis onset.
Answer: Irreversible proteolysis of key regulators (for example, cyclins) via APC/C. Once cyclins are destroyed, the process cannot reverse until new synthesis occurs.
Answer: A commitment point in late G1 after which the cell proceeds to S phase. Once passed, cells are committed to completing the division cycle.
Answer: Wee1 kinase. Checkpoint kinase maintains G2 arrest when needed.
Answer: Spindle assembly checkpoint. Monitors attachment status before allowing progression.
Answer: Crowding reduces division via cell-cell contact and signaling. Contact inhibition prevents overgrowth when cell density becomes too high.
Answer: G0 phase. Quiescent state where cells exit the cycle but remain metabolically active.
Answer: Inhibits the cell cycle; tumor suppressor. Retinoblastoma protein blocks $G_1$/S transition.
Answer: Cytokinesis. Physical division of cytoplasm creates two cells.
Answer: Spindle assembly checkpoint. M checkpoint ensures proper chromosome attachment.
Answer: Cyclin D. Early cyclin promotes entry into S phase.
Answer: Failure to enter anaphase due to securin and cyclin persistence. Unable to degrade key proteins required for anaphase progression and mitotic exit.
Answer: p53 protein. Activates apoptotic pathway when damage is severe.
Answer: Premature checkpoint bypass and increased uncontrolled proliferation. Removes normal cell-cycle brakes, leading to continuous proliferation signals.
Answer: G₀ phase. Quiescent state for non-dividing differentiated cells.
Answer: It degrades ubiquitin-tagged regulatory proteins (for example, cyclins). Destroys cell-cycle regulators to ensure unidirectional progression through phases.
Answer: Aneuploidy due to improper chromosome segregation. Unequal chromosome distribution causes genomic instability.
Answer: The G2 checkpoint. Prevents mitosis when DNA replication errors or damage are detected.
Answer: Telophase. Final mitotic phase reverses nuclear breakdown.
Answer: G₁ phase. Gap phase for organelle synthesis and growth.
Answer: G1 phase. Cell accumulates materials and energy needed for DNA replication and division.
Answer: It is a CDK inhibitor that blocks cyclin-CDK activity. Blocks S-phase gene transcription by preventing E2F transcription factor activity.
Answer: Wee1 kinase. Checkpoint kinase maintains G2 arrest when needed.
Answer: G₂/M checkpoint. Prevents mitosis with damaged or unreplicated DNA.
Answer: Inhibits CDKs, acting as a checkpoint regulator. CDK inhibitor enforces $G_1$/S checkpoint arrest.
Answer: Programmed cell death that removes damaged or abnormal cells. Eliminates cells with irreparable damage that could bypass cell-cycle controls.
Answer: Spindle assembly checkpoint. Monitors attachment status before allowing progression.
Answer: A gene whose loss of function removes restraints on cell division. Normally acts as brake on cell division; loss promotes cancer development.
Answer: Cyclin-dependent kinases (CDKs). Phosphorylate target proteins when bound to cyclins.
Answer: Cell-cycle arrest in G1 due to continued inhibition of E2F. Rb remains active and blocks E2F, preventing S-phase gene expression.
Answer: A control point that can pause progression until conditions are correct. Ensures proper order and prevents errors by monitoring completion of previous events.
Answer: After S phase (during G2 and early M). Sister chromatids remain attached until anaphase when cohesin is cleaved.
Answer: Cell cycle arrest until DNA repair is complete. Halts progression until repair mechanisms finish.
Answer: Separase. Protease cleaves cohesin rings holding chromatids.
Answer: Spindle assembly checkpoint. M checkpoint ensures proper chromosome attachment.
Answer: Accelerated entry into S phase. Excessive cyclin E bypasses normal checkpoint control.
Answer: Loss of contact inhibition (reduced density-dependent inhibition). Cancer cells continue dividing despite crowded conditions that stop normal cells.
Answer: They phosphorylate target proteins to drive cell-cycle transitions. Phosphorylation activates substrates that control key transitions like S-phase entry or mitosis onset.
Answer: G1 phase. Cell accumulates materials and energy needed for DNA replication and division.
Answer: G₁/S checkpoint. Restriction point prevents replication of damaged DNA.
Answer: Loss of contact inhibition (reduced density-dependent inhibition). Cancer cells continue dividing despite crowded conditions that stop normal cells.
Answer: Nuclear envelope breakdown. Nuclear membrane dissolves for spindle access.
Answer: Cells must attach to a surface (ECM) to progress through the cell cycle. Prevents division of cells that have lost proper tissue contact.
Answer: Regulate the progression of the cell cycle. Oscillating proteins that activate CDKs at checkpoints.
Answer: Cyclin D. Early cyclin promotes entry into S phase.
Answer: A normal gene that can become an oncogene when mutated or overexpressed. Encodes proteins that normally promote controlled cell division and growth.
Answer: A commitment point in late G1 after which the cell proceeds to S phase. Once passed, cells are committed to completing the division cycle.
Answer: G0 phase. Quiescent state where cells exit the cycle but remain metabolically active.
Answer: They provide external signals that stimulate passage through G1. Signal adequate nutrients and conditions for cell division to proceed.
Answer: To ensure accurate DNA replication and cell division. Prevents genetic defects by controlling division timing.
Answer: p53. Guardian of the genome that responds to DNA damage by activating checkpoints.