Bio 230

animal organelles that “nucleate” microtubules that make up the spindle

• Microtubules = polymer
• Tubulin = monomer

region where sister chromatids are connected (DNA)

protein structure on chromatids where the spindle fibers attach during cell division to pull sister chromatids apart

Separate pieces of DNA in a cell

identical pieces of DNA held together by a centromere

• Euchromatin (no condensed chromosomes)
• Nuclear membrane still present
• Microtubules at the cell periphery

Protein based organelle

• 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

• Late prophase !!!
• Everything is HC
• Nuclear membrane is gone
• Microtubules can now interact at kinetochore, which is present at both sides of replicated chromosomes

• 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

• Separate sister chromatids
• NM dissolved
• Microtubules pull chromatids to the poles (opposite side of spindle)

• Decondense DNA —> becomes euchromatin
• Decrease amount of microtubules
• New NM forms around segregated chromosomes

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

• 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

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.

• 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

• G1 S
• G2 M
• Metaphase  anaphase

• 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

• —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

• Mitogens: molecules that stimulate cells from G0  G1
• Mitogens bind to receptors and turn on signaling pathways
• —Target is often activation of transcription factors

• Proto-oncogene: functionally normal to promote cell cycle
• Oncogene: promotes cell cycle when it should not
• Tumor Suppressor: cause cancer when they are inactivated

• —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

• 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

• 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

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