Bio 230

  1. Centrosome
    animal organelles that “nucleate” microtubules that make up the spindle

    • Microtubules = polymer
    • Tubulin = monomer
  2. Centromere
    region where sister chromatids are connected (DNA)
  3. Kinetochore
    protein structure on chromatids where the spindle fibers attach during cell division to pull sister chromatids apart
  4. Chromosome
    Separate pieces of DNA in a cell
  5. Chromatid
    identical pieces of DNA held together by a centromere
  6. Interphases
    • Euchromatin (no condensed chromosomes)
    • Nuclear membrane still present
    • Microtubules at the cell periphery
  7. Microtubules
    Protein based organelle
  8. Prophase
    • heterochromatin (chromosomes now present, chromosomes = most compact form of DNA)
    • Nuclear membrane still present
    • Microtubules are starting to increase but they’re still in the periphery

    As we enter mitosis, dna associates with histones more to form heterochromatin and ultimately chromosomes
  9. Prometophase
    • Late prophase !!!
    • Everything is HC
    • Nuclear membrane is gone
    • Microtubules can now interact at kinetochore, which is present at both sides of replicated chromosomes
  10. Metaphase
    • Chromosomes line up at division plate/metaphase plate
    • NM is still dissolved
    • All kinetochores attached to microtubules
    • — if one kinetochore doesn’t attach —> aneuploidy: abnormal # of chromosomes
  11. Anaphase
    • Separate sister chromatids
    • NM dissolved
    • Microtubules pull chromatids to the poles (opposite side of spindle)
  12. Telophase
    • Decondense DNA —> becomes euchromatin
    • Decrease amount of microtubules
    • New NM forms around segregated chromosomes
  13. Define “dynamic instability” of microtubules and how it relates to the structure and function of microtubules.
    Dynamic instability is the switching between growing (poly- merizing) and shrinking (depolymerizing) states

    • MTs typically grow (polymerize) from + end and shrink (depolymerize) from – end
    • If – end is stabilized, the + end CAN depolymerize

    • Beta (+): very active, less stable (monomers can add & subtract)
    • Alpha (—): more stable, less active
  14. Identify the different microtubules that create the mitotic spindle and describe their function.
    • Kinetochore: responsible for chromosome movement
    • Polar microtubules: contribute to cell elongation and cell stability by overlapping
    • Astral microtubules: grow toward the membrane of the cell
  15. Discuss how acentrosomal organisms (like plant cells) can still form a functional spindle.
    chromatin and nuclear membrane can act as mictotubule organizing centers

    Motor proteins will help organize the microtubules that are made from chromatin or nuclear envelope in plant cells. In animal cells, motor proteins help organize the microtubules that are made from centrioles or chromatin.
  16. Compare and contrast the three different models of spindle formation: “search and capture”, “chromosome-drive” and “search and transport” (Sci Lit - Week 7).
    • Search and capture: microtubules only seek out
    • kinetochores

    Search and transport: microtubules find both kinetochores and other microtubules

    Chromosome driven: means that the chromatin can act as a microtubule organizing center to help nucleate chromosome
  17. Describe the timing of the three major checkpoints in relation to the cell cycle and what they are monitoring.
    • G1 S
    • G2 M
    • Metaphase  anaphase
  18. Compare and contrast cyclins and cyclin-dependant kinases
    • CDKs – cyclin-dependent kinases
    • —Activated CDKs will phosphorylate targets
    • —Promote progression through the cycle
    • —Cycle concentration increases during mitosis and decreases in interphase

    • Cyclins (D, E, A, B)
    • —CDK regulators
    • —CDK + cyclin = activated complex

    • CDK levels are typically constant during the cell cycle, while cyclin levels fluctuate
    • This results in certain CDK:cyclin complexes to be active during specific times
  19. How do CDKs and cyclins function
    • —Binding of cyclin to CDK causes a conformational change to CDK which Allows phosphorylation of amino acid in active site
    • —Active cyclin:CDK complexes phosphorylate additional target proteins to promote cell cycle progression
  20. Define mitogen (example myc) and entry into the cell cycle.
    • Mitogens: molecules that stimulate cells from G0  G1
    • Mitogens bind to receptors and turn on signaling pathways
    • —Target is often activation of transcription factors
  21. Compare and contrast proto-oncogene, oncogene and tumor supressor genes.
    • Proto-oncogene: functionally normal to promote cell cycle
    • Oncogene: promotes cell cycle when it should not
    • Tumor Suppressor: cause cancer when they are inactivated
  22. Describe the role of p53 and p21 in the cell cycle (Worksheet 15).
    • —is activated during cell “stress” such as DNA damage
    • —is a transcription factor that upregulates other “p” proteins (like p21)
    • —is a tumor suppressor gene
    • —Deregulation removes suppression and uncontrollable division can occur

    If replicated DNA is damaged, p53/p21 proteins inhibit progression

    p21 blocks any CDKs from binding their partner cyclins
  23. Explain how the balance of kinases and p-proteins affects the cell cycle.
    • More Kinase activity (No stress/DNA damage signal
    • Less p-protein activity
    • =Progression trough transition

    • More p-protein activity (stress/DNA damage signals present)
    • Less Kinase activity
    • =Inhibition of the cell cycle/pause at checkpoints
  24. Describe the metaphase checkpoint (Worksheet 16) including identifying all major proteins (cohesin, separase, securin, APC, cdc20, Mad/Bub) involved in the process.
    • Cohesion: hold sister chromatids together
    • Separase: degrades the protein,cohesion, and degrades cohesion b/t chromatids
    • APC: anaphase promoting complex — activates separase, breaksdown securin so it can release seaparase
    • cdc20: activates APC, point of regulation for the metaphase checkpoint.

    • So no inhibitorsAnaphase
    • inhibitorsno Anaphase

    Mad/Bub: cdc20 inhibitors, inhibit cdc20
  25. Signal
    The "signal" in the metaphase checkpoint are the MAD2 and BubR1 proteins. Remember they are activated when the microtubules (MTs) are NOT attached to the kinetochores. The two proteins I mentioned are also called APC-inhibitor proteins.

    • High metaphase checkpoint signal = MAD2 and BubR1 proteins are inhibiting Cdc20 from interacting with APC
    • Low metaphase checkpoint signal = MT's are attached to kinetochores

    If metaphase checkpoint signal is on = anaphase stop signal
Author
user011
ID
351333
Card Set
Bio 230
Description
Updated