Test Ch 18 (You Got THis) Flashcards
(16 cards)
Discuss the importance of cell division cycle control and cell death
Cell division cycle control ensures that cells divide only when conditions are favorable (enough nutrients, no DNA damage, correct size) and only when needed.
Without regulation, cells would divide uncontrollably, leading to cancer.
Cell death (apoptosis) balances division. It removes damaged or unnecessary cells without causing inflammation. Proper regulation of cell death is crucial for normal development, tissue maintenance, and preventing cancer.
Diagram the cell division cycle and describe the overall events in each phase of the cycle: G1, S, G2 and M.
Phases:
G1 Phase: Cell grows, produces RNA and proteins needed for DNA replication. Prepares for S phase.
S Phase: DNA replication occurs. Each chromosome duplicates to form two sister chromatids.
G2 Phase: Further cell growth; prepares all necessary proteins for mitosis.
M Phase: Includes mitosis (nuclear division) and cytokinesis (division of the cytoplasm into two cells).
Diagram (simple version):
G1 → S → G2 → M
Describe the experimental evidence that led to the discovery of M-Cdk and cyclins.
Key experiment:
Frog egg extracts from cells in M phase were injected into oocytes.
These extracts forced the oocytes into M phase even if they were not ready.
This showed there was a soluble factor in dividing cells — later called Mitosis Promoting Factor (MPF).
Scientists later purified MPF and found it contained a protein kinase (M-Cdk) and a regulatory subunit (cyclin).
Describe and diagram the change in M-Cdk and cyclin concentrations and activity during the cell cycle.
Cyclin concentration gradually rises through interphase (G1, S, G2) and peaks in M phase.
M-Cdk activity is off even when cyclin levels are high because it’s kept inactive by phosphorylation.
Activation happens abruptly at the start of mitosis when Cdc25 phosphatase removes inhibitory phosphates.
After mitosis, cyclin is degraded rapidly by the APC/C complex, turning M-Cdk activity off.
Simple graph sketch:
Cyclin: slow rise → sudden drop
M-Cdk activity: stays low → sudden spike at mitosis → sudden fall after mitosis
Describe the role of inhibitory kinase Wee1 and activating phosphatase Cdc25 and Anaphase Promoting Complex (APC/C) in regulating M-Cdk activity.
Wee1 kinase: adds inhibitory phosphates onto M-Cdk, keeping it inactive.
Cdc25 phosphatase: removes inhibitory phosphates, activating M-Cdk to trigger mitosis.
APC/C (Anaphase Promoting Complex): adds ubiquitin chains to cyclins, marking them for destruction by the proteasome — this inactivates M-Cdk and allows mitosis to end.
. Discuss the purpose of cell-cycle checkpoints and give examples.
Purpose:
To pause the cell cycle if conditions aren’t right, preventing damaged DNA or incomplete replication from being passed to daughter cells.
Examples:
G1/S Checkpoint: Ensures DNA is not damaged before replication. (p53/p21 pathway)
G2/M Checkpoint: Ensures all DNA is replicated correctly before mitosis.
Spindle Checkpoint (Metaphase Checkpoint): Ensures all chromosomes are attached to spindle before anaphase begins.
Discuss the role and the mechanism of control of the cell cycle by p53/p21.
If DNA is damaged (e.g., from radiation), sensors activate p53.
p53 becomes active and turns on the transcription of the p21 gene.
p21 protein is made and inhibits G1/S-Cdk and S-Cdk by binding to them.
This stops DNA replication, allowing time for DNA repair.
If the damage is too severe, p53 can trigger apoptosis.
p53 is a tumor suppressor; over 50% of human cancers have mutations in p53.
Define and discuss the importance of G0. Describe how and why a cell enters or leaves G0.
G0 phase: A resting, non-dividing state.
If the cell doesn’t receive growth signals at the G1 checkpoint, it enters G0.
In G0:
Cyclins and Cdks disappear.
The cell may stay there for days, years, or forever (e.g., neurons).
Cells re-enter the cycle from G0 if they receive mitogenic signals.
G0 is important to prevent unnecessary division and maintain tissue function.
. Discuss the role of mitogens in cell cycle control and the mechanism by which Rb effects the cell cycle.
Mitogens are external signals (like growth factors) that stimulate cells to divide.
Mitogens activate Cdks, which phosphorylate Rb protein.
Rb (Retinoblastoma protein) normally binds and inhibits transcription factors that are needed for S phase.
When phosphorylated, Rb releases these transcription factors, allowing the cell to proceed into S phase and divide.
Identify and describe the cellular events in the stages of mitosis.
Stages:
Prophase: Chromosomes condense; mitotic spindle begins to form.
Prometaphase: Nuclear envelope breaks down; spindle attaches to kinetochores.
Metaphase: Chromosomes align at the metaphase plate (equator).
Anaphase: Sister chromatids separate and move to opposite poles.
Telophase: Nuclear envelope reforms; chromosomes decondense.
Cytokinesis: Cytoplasm divides via contractile ring (actin + myosin).
Describe steps during mitosis that are directly affected by M-Cdk.
M-Cdk phosphorylates:
Condensins → triggers chromosome condensation.
MAPs (Microtubule Associated Proteins) → increases dynamic instability of microtubules for spindle formation.
Nuclear lamins → causes nuclear envelope breakdown.
Cdc25 → positive feedback activation of more M-Cdk.
Thus, M-Cdk controls chromosome condensation, spindle formation, and nuclear envelope breakdown.
Describe the role of cohesins, condensins and anaphase promoting complex (APC/C) in chromosome structure during mitosis.
Cohesins: Proteins that hold sister chromatids together after DNA replication.
Condensins: Proteins that compact chromosomes during prophase.
APC/C:
Ubiquitinates securin, freeing separase to cleave cohesins at anaphase.
Also triggers cyclin destruction to end mitosis.
Describe the roles of microtubules, intermediate filaments and actin filaments in M phase.
-Microtubules:
Form the mitotic spindle.
Pull apart sister chromatids.
-Intermediate filaments (nuclear lamins):
Their breakdown by M-Cdk causes nuclear envelope breakdown.
Reformation during telophase.
-Actin filaments + myosin:
Form the contractile ring for cytokinesis, physically dividing the cell into two.
Describe and diagram the formation of and structure of the complete mitotic spindle and how it functions during each stage of mitosis, including the roles of motor proteins.
-Formation:
~MTOCs (centrosomes) duplicate during S phase.
~Spindle fibers (MTs) grow from centrosomes.
~Spindle fibers attach to kinetochores on chromosomes.
-Motor proteins (kinesin, dynein):
~Move chromosomes along microtubules.
~Separate poles during anaphase.
-Spindle MT types:
~Kinetochore MTs: Attach to kinetochores.
~Interpolar MTs: Overlap and push against each other.
~Astral MTs: Radiate out to cell cortex to anchor spindle.
Define apoptosis, describe its importance and compare it to necrosis.
Apoptosis: Programmed, controlled cell death; no inflammation; cell contents neatly packaged for phagocytosis.
Necrosis: Accidental, messy cell death; causes inflammation because contents spill out.
Apoptosis shapes organs, removes defective cells, and prevents cancer.
Describe the role of caspases in apoptosis and how caspase activity is regulated by Bcl2 family of proteins (Bak and Bax).
Caspases are proteases that cleave cellular proteins during apoptosis.
Initiated as inactive procaspases, which are cleaved to become active.
-Bcl2 family proteins:
Bak and Bax promote apoptosis by causing mitochondria to release signals that activate caspases.
Anti-apoptotic Bcl2 proteins block Bak and Bax to prevent apoptosis unless needed.
