Foundations of Biology Exam 3: Cell Cycle Control

G2 checkpoint

pass checkpoint if:

1. chromosomes have replicated successfully

2. DNA is undamaged

3. activated MPF is present

metaphase checkpoint

pass checkpoint if:

1. chromosomes have attached to spindle apparatus

2. chromosomes have properly segregated and MPF is absent

G1 checkpoint

pass checkpoint if:

1. cell size is adequate

2. nutrients are sufficient

3. social signals are present

4. DNA is undamaged

resource

maintaining specific cell density ensures organisms can keep up with __________ demands

cyclin

protein produced by a cell after cell signaling growth factors arrive; activates Cdk; needed for cell to move past G1 checkpoint

Cdk

activated by cyclin phosphorylating it and removing its inactivating phosphate; goes on to phosphorylates Rb; important to get past G1 checkpoint

step 1 in passing G1 checkpoint

growth factors arrive from other cells

step 2 in passing G1 checkpoint

stimulation from growth factors cause cells to produce cyclin and E2F

step 3 in passing G1 checkpoint

cyclin binds and phosphorylates Cdk and Rb inactivates E2F by binding to it

step 4 in passing G1 checkpoint

Cdk phosphorylates Rb after inactivating phosphate is removed

step 5 in passing G1 checkpoint

phosphorylated Rb releases E2F

step 6 in passing G1 checkpoint

E2F triggers production of S-phase proteins

P53 proteins

proteins that signal to stop the cell cycle if DNA is damaged at G1 checkpoint; create Cdk inhibitors

fates of cells paused in G1 phase

1. DNA repair

2. senescence

3. cell death

mutagens

cause cell damage; ex. chemicals, UV radiation, x-rays

UV light

exposer to ____ ________ reduces and stops cell division

nucleotide excision repair

DNA repair mechanism:

1. a complex of proteins detect irregularity in DNA structure

2. an enzyme nicks DNA on both sides of the damage

3. a DNA helicase unwinds and removes the region with the damaged bases

4. DNA polymerase fills the gap in 5'-3' direction using the template strand

5. DNA ligase links the new strand to the pre-existing strand

uvrA

protein that recognizes DNA damage and signals to start repair mechanisms

recA

protein that facilitates DNA repair

telomeres

act as a buffer for chromosomes following DNA replication; has a repetitive sequence (TTAGGG); no genes in this region; end up being cut off slowly

the problem with lagging strands

DNA polymerase cannot replicate the ends of the lagging strand because there is no 3'-OH for covalent extension; ends up getting cut off

hayflick limit

the average number of times a normal human cell population will divide before becoming senescent and dying

cannot

once telomeres are gone, the cell _______ pass the G1 checkpoint because cell division would cause loss of protein coding DNA at ends of chromosomes

telomerase

an enzyme that contains an RNA primer and restores telomere length; maintain replicative capacity of cells; humans loos this enzyme during embryonic division

DNA polymerase

99% of mismatched DNA is recognized and removed by ____ __________; mismatches are recognized by their abnormal hydrogen bonds

MPF

the name of the active cyclin-CDK complex that initiates mitosis or M-phase

cyclin

MPF activity increases as a cell makes more _______

MPF activation

_____ __________ initiates mitosis

cancer

disease of the cell cycle; do not go through programmed cell death

common set of behaviors in cancer cells

- proliferate unchecked by the cell cycle checkpoints

- re-express telomerase

- can create blood vessels to get access to resources like glucose and oxygen

- increase mutations that support cancer

- can continue to function abnormally by evading cell death

BRCA1 mutation

_____ __________ is often a predictor of cancer; this gene codes for an enzyme that fixes DNA damage

quinolones

inhibit topoisomerase (and other DNA stabilizing proteins) to disrupt DNA synthesis; if no new DNA can be synthesized, cells will stop dividing; cancer treatment

taxol

destabilizes microtubules to stop division during M phase; stops microtubules from moving; treats cancer by stopping cell division

stathmin

promotes depolymerization and prevents polymerization; stops microtubules from forming; treats cancer by stopping cell division