Lecture 26

Question 1

post mitotic

Answer 1

never divide

Question 2

cell cycle

Answer 2

M1 to s to m2 to g
-driven by cyclin levels that go up and down

Question 3

how did we find the cell cycle

Answer 3

in yeast that we stained blue
-also found restrictive temperatures

Question 4

22 celsius

Answer 4

permissive temperature that allows cell cycle

Question 5

36 celsius

Answer 5

restrictive temp no division
-temp sensitive mutations control the genese

Question 6

CDC28 gene

Answer 6

in yeast regulates and encodes cyclin dependant kinase and regulate cell cyclin

Question 7

CDK CYCLIN

Answer 7

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

Question 8

check points

Answer 8

g1 g2 and M

Question 9

g1 to s progression stopped by

Answer 9

DNA damage

Question 10

what triggers repair at g1 to s

Answer 10

p53 which will express p21 that will inhibit cdk to stop the cycle

Question 11

what happens if chromosomes dont attach to spindle correctly

Answer 11

pause between metaphase and anaphase

Question 12

cancer can keep dividing because

Answer 12

it makes more telomerase and dont respond to cell cycle control
-have messy chromosomes

Question 13

tummor suppressors

Answer 13

are the brakes of the cell cycle
-RB will block E2F from synthesizing DNA
-p53 forces repair or apoptosis

Question 14

what happnes when suppresors get lof

Answer 14

eventually you will get an oncogene mutation becuase we cant put a break on the cell cycle to stop a mutation from proliferation

Question 15

oncogene GOF mutation

Answer 15

drive cell division
-proto oncogene (normal) becomes constitutive

Question 16

RAF mutation

Answer 16

changes in signal pathway, not a repressor

Question 17

oncogenes mimic?

Answer 17

growth factor stimulation that will promote cell division

Question 18

growth factor mutations

Answer 18

7 less and c elegan

Question 19

RAS mutation

Answer 19

dont need growth factor for mutation, will activate phosphorylationc ascade

Question 20

mutations at receptor

Answer 20

thinks ligand is present when it is not or kinase never turns off

Question 21

oncogene mutations

Answer 21

translocation, point mutation anad amplification

Question 22

translocation

Answer 22

new promoter
-philadelphia chromosome transplants abl to control bcr promoter
-mimics growth factor
-leukemia
-bcl prevents apoptosis causing b cell lymphoma

Question 23

amplification

Answer 23

too much growth protein

Question 24

inherited cancer

Answer 24

from suppressor mutation
-hets are only one mutation away from RB LOF
-2 hit model

Question 25

mutli hit model

Answer 25

multiple mutations over time