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BMS 2 > Regulation of Cell Division > Flashcards

Regulation of Cell Division Flashcards

1
Q

to replicat

A

late g1-s cyclins transcribed
s cyclin binds to cdk-s/cdk/cyclin complex
late g1-pre-rc compelx-orc , cdcbound, mcm (recruted by cdc binding to orc)
s/cdk/cyclin phosphorylases cdkb+ORC
cdcb phosphortalted and degraded
mcm able to act as helices, exits nucleus
DNA pol+machinery recruited
cdcb and mcm leave
-cdcb phosphorylated through g2
go back to this after slides

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2
Q

Internal vs external controls

A

internal-monitors cell cycle progression, make sure occur in step wise succession

external-stimultate cell division when more cells needed-block when they are not

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3
Q

use of g1/g2

what parts are part of interphase

A

time delay for cells to grow-accumulate mass

time delay for monitoring intra/extra cellular conditions

G1, g2, and s

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4
Q

Restriction point

what if not favorable

A

@ end of G1-measures favorability of environemnt

  • passes restribction point and is COMMITTED TO DNA REP
  • cant go back if go past this point even if conditions are unfavorable

enter g0

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5
Q

important features of cell cycle control (4)

A

certain time to turn on specific event

initate events in correct order

make sure each event is only triggered 1x per cell cycle

on/off switches-trigger events in complete/reversible style

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6
Q

what happens when enter s, m, leave m

A

trigger DNA rep machinery

trigger mitosis machinery

trigger cytokinesis

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7
Q

cyclin depedent kinase

A

CDK

activity increases/decreases at different stages of cell cycle

leads to phosphorylation of different proteins at different times in cell cycle-inittates/regs key events

Dependnt on cyclins for kinase activity

Different cyclins for different parts of cell cycle

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8
Q

mCDK vs sCDK

A

spindle assembly + other mitosis machinery turns on

enzymes for replication are phosphorylated (activated)

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9
Q

4 classes of cdks + associated cyclin

A 
g1-promtes passage through restriction point
-cyclin D
g1/s-commits cell to replication
-cyclin E
s-intitates replication
-cyclin A
m-promotes mitosis
-cyclin B
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10
Q

molecular swtich

A

cyclin/cdk-initiate different steps of cell cycle

  • poised for activation
  • recieve signal to become fully activated (usually phosphorylation)
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11
Q

how ensure switches fire in correct order/fire once per cycle?

A

feedback mechanisms

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12
Q

S-cdk control + function

A

controls initiation of DNA replication once per cell cycle at replication origins

Origins of replication-origins of replication-large multi-protein complex binds here

s cyclin transcribed in late g1

s-cdk activated-phosphorylates cdc6_preRC
-point of no return

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13
Q

ORC

A

binds throughout cell and acts as landing pads for other reg proteins-initiate replication at different positions throughout the genome

binds early g1

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14
Q

pre replicative complex

A

cdc6 and orc

Mcm comes in (helices)
-together with all 3-posited to go if environemnt favorable

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15
Q

Phosphorylation of Cdc6

phosphorylation of orc

A

degradation

by s-cdk

fucking draw slide 24

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16
Q

How is invitiation of entry to S phase controlled (3 parts)

A

CDC6

  • usually present at low levels throughout cell cycle-but increasingly transiently in early g1
  • binds to ORC-causes recruitment of Mcm protein which are helices
  • ORC, CDC6, MCM make pre-RC-poised to replicate DNA

s-cdk

  • iniitated by expression of s-cyclin
    • phosphorylation
  • assembles DNA polymerase and other replication machinery at the origins
  • activate the mcm proteins to slide along the DNA and act as helices
  • phosphorylates mcm proteins and causes thier export from the nucleus
  • upon completion-no cdc6 and no mcm

S cyclin

  • origin is now ready to fire-requires activity of S-CDK
  • S-cyclin transcription is activated in late G1
    • S cdk inactive without s-cyclin present
  • s cyclin -cdk complex forms activating s-cdk that then phosphorylates pre-RC activating it for replication
    • does this by degrading cdc6 in pre-RC
  • complex then can recruit poly _other machinery+allow mcm to do helices activity
17
Q

S cdk prevents re-replication

A

Phosphorylation of cdc6 by S-cdk causes cdc6 to dissocatite from ORC-after origen fired for replication
-disassembly of pec-prevents replication from occurring at same origin

Dissocatio nand phophrylation of Cdc6 from ORC causes its degradation

S-cdk phosphorylates Mcm/helicase proteins and cause their export from nucleus

draw slide 28

18
Q

ways to prevent re-replication

A

S-cdk activity remains high in G2 and mitosis causes Cdc6 protein to be always phosphorylated and therefore prevents re-replication

M-cdk-phosphorylat]es Cdc6 and MCM

19
Q

How does cell cycle control system reset itself to allow replication

A

At end mitosis -Cdk activity is reduced to zero

  • no CDK to phosphoryylate Cdc6+CM
  • new Cdc6+mcm made in net cell cycle-wont be phosphorylated

results in dephosphorylted Cdc6 and MCM proteins allowing pre-RC assembly to occur again

20
Q

Triggering entry to mitosis (3 proteins)

A

Activation of M cyclin

Have a system tha is poised and ready to go

M cyclin-gradually increases during G2 and M phases

CAK-Cdk activating Kinase

Wee1-Cdk inhibitory kinase

draw slide 31

21
Q

CAK

A

Cyclin activates CDK conformational change to expose active t-loop

CAK comes in and phosphorylates t-loop

22
Q

Wee1

A

CDK activating phosphate
-Wee1 adds another phosphate-inhibits

  • poised for activation-just need to take off inhibitory phosphate
  • done by cdc25
23
Q

M-cdk

A

phosphorylates proteins that are responsible for assembly of simple, chromasome condensation, breakdown of nuclear envelope

24
Q

Feedback of M-cdk

A

M-cdk inhibits Wee1 causing more activated M-cdk to form

M cdk phosphorylates more cdc25 activting more phosphatase that leads to more actived m-cdk

25
Q

Inactivation of m-cdk

A

allows for exit of mitosis

APC+Cdc20-creates active APC

 - CATALYYZED BY M-CDK - add ubiquitin to M-clyclin-degredation in proteasome
26
Q

G1 phase is characterized by+mechanisms to ensure this

A 
absence of Cdk activity
=ubiquitin mediated degradation of sdks
=cyclin kinase inhibitor accumulation
=decreased cyclin transcription
  -mediated by retinoblastoma protein and E2F transcription factor
27
Q

why is there not cdi in g1

A

increased cki activity (p27), and increased rb

28
Q

p27 (or 21…?)`

A

a ck. that bind and inactivates active cyclin-cdk complex

-expression stimulated by p53

29
Q

decreased cyclin transcription is caused by

A

Rb protein

E2F is a TF that regulates expression of many genes required for entry into s phase including G1-S and S cyclins

  • controlled in part by Rb protein
    • during G1, Rb binds to E2F and blocks its activity
    • results in downstream genes (G1/S and S cyclins) not being transcribed

When cells receive an extra-cellular signal to divide, G1-Cdk accumulates, phosphorylates Rb, and reduces affinity of Rb to E2F which results in expression G1/S and S cyclins

Retinoblastoma-Less than two copies of Rb gene

DRAW 42/44

30
Q

Rb feedback loops

A

EfF is released by Rb inactivation, E2F then increases its own expression

E2F expression leads to production of G1/S-cdk and S-cdk
-phosphorylates more Rb and released E2F

Increase on G1/CDK and S-CDk activities enhances the phosphorylation of ubiquitin ligases and CKIs, leading to thier destruction i nproteosome and as a consequence activate G1/s-Cdk and S cdk

31
Q

DNA checkpoints

A

late g1 and late g2

32
Q

g2 checkpoint

A

DNA damaged in late g2 before mito

Damaged DNA send signal that blocks cdc25 activity
cdc25 removes inhibitory phosphate put on by wee1

33
Q

p53 and g1 dna damage checkpoint

A

g1 prevents progression into S by inhibiting activation of g1/scdk and s cdk complexes
-controlled partially by p53

p53 stimulates expression of several gens including CKI protein (p21)

BMS 2 (41 decks)

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