Lecture 26 Flashcards
post mitotic
never divide
cell cycle
M1 to s to m2 to g
-driven by cyclin levels that go up and down
how did we find the cell cycle
in yeast that we stained blue
-also found restrictive temperatures
22 celsius
permissive temperature that allows cell cycle
36 celsius
restrictive temp no division
-temp sensitive mutations control the genese
CDC28 gene
in yeast regulates and encodes cyclin dependant kinase and regulate cell cyclin
CDK CYCLIN
cyclin bind to cdk and activate kinase activity
-when it phosphorylates it activates different substrates that will regulate cell cycle
-self regulate by making the enzymes that degrade them
check points
g1 g2 and M
g1 to s progression stopped by
DNA damage
what triggers repair at g1 to s
p53 which will express p21 that will inhibit cdk to stop the cycle
what happens if chromosomes dont attach to spindle correctly
pause between metaphase and anaphase
cancer can keep dividing because
it makes more telomerase and dont respond to cell cycle control
-have messy chromosomes
tummor suppressors
are the brakes of the cell cycle
-RB will block E2F from synthesizing DNA
-p53 forces repair or apoptosis
what happnes when suppresors get lof
eventually you will get an oncogene mutation becuase we cant put a break on the cell cycle to stop a mutation from proliferation
oncogene GOF mutation
drive cell division
-proto oncogene (normal) becomes constitutive
RAF mutation
changes in signal pathway, not a repressor
oncogenes mimic?
growth factor stimulation that will promote cell division
growth factor mutations
7 less and c elegan
RAS mutation
dont need growth factor for mutation, will activate phosphorylationc ascade
mutations at receptor
thinks ligand is present when it is not or kinase never turns off
oncogene mutations
translocation, point mutation anad amplification
translocation
new promoter
-philadelphia chromosome transplants abl to control bcr promoter
-mimics growth factor
-leukemia
-bcl prevents apoptosis causing b cell lymphoma
amplification
too much growth protein
inherited cancer
from suppressor mutation
-hets are only one mutation away from RB LOF
-2 hit model
mutli hit model
multiple mutations over time
