Flashcards in 9-15 Cell Cycle I Deck (24):
Name the 4 Phases of the cell cycle
1) M PHASE
INTERPHASE (Continuous Cell Growth) PARTS:
2) G1 phase Go
3) S Phase [DNA replication]
4) G2 phase
What is the order of division within the M Phase
1st: Nuclear Division //
2nd: Cytoplasmic Division (Cytokinesis)
What are the common cell cycle checkpoints for G2 CheckPoint / Entering ___ PHASE ? 
Entering M Phase / G2 checkpoint:
1-Is all DNA replicated
2- DNA damage?? If so= CELL CYCLE ARREST
3-Is environment favorable
Common Cell cycle checkpoints for G1 Checkpoint / Entering ____ phase? 
2)Why is this checkpoint different from others?
Entering S phase / G1 checkpoint:
A: MOST IMPORTANT CHECKPOINT/SIGNAL=dictates [Divide or Die]
B: Is environment favorable?
2) Different because there is no going back and this is the [Divide or Die] decision checkpoint based on growth of mitogenic factors. +Growth = Divide /S phase
Common cell cycle checkpoints for Mitotis Checkpoint / Leaving ____ Phase
Metaphase Checkpoint / Leaving M PHASE
1) Are all chromosomes attached to spindle?
IF NOT = Anaphase WILL NOT proceed in normal cells
The Control/Checkpoint system of Cell Cycles ensures what 4 things
1. Proper timing
2. Correct Order
3. Feedback mechanisms
4. Phases only occur ONCE per cell cycle
Cdk(___ ___ ___) relies on ___ binding for it to become activated.
2) What are these CdK responsible for?
3)When are these CdK degraded in a cell cycle?
4) When are Cyclins degraded?
CdK(Cyclin-Dependent Kinase) relies on Cyclin[different in each cycle] to bind to it for it to be ACtivated!
2)Cdk turns on different phases of the cell cycle and are different for each phase (like Cyclins)
3) CdK is NOT degraded until the [Go] phase! Otherwise, they stay around for the entire ride!
4) After a cyclin has done its duty, its levels drop down when entering a new phase
[T or F] Concentrations of the 3 major CYCLINS does NOT oscillate during the cell cycle.
FALSE! the 3 major CYCLINS have concentrations that DO oscillate during the cell cycle while... Cdk conc. stays constant and ends up exceeding cyclin amount until [Go].
In regards to Cyclins and Cdk, war happens in Late G1 / almost S-phase?
[Divide or Die] check point is passed 1st and then rising
G1/S-cyclin levels bind and lead to activation of G1/S-Cdk which triggers progression thru the start checkpoint!
In regards to Cdk what actually triggers DNA replication and "some" early mitotic events?
S-Cdk (after being activated by S-cyclins) form at start of S-phase and trigger DNA replication as well as some "early" mitotic events
1-When do M-Cdk form?
2-When are M-Cdk activated and what do they do?
3) What does APC/C do?
1)M-Cdk forms DURING G2 phase but held inactive until the end of it
2) M-Cdk are activated AT THE END OF G2 and officially trigger early events of mitosis. >>>M-Cdk is turned off when APC/C starts because APC/C destroys M-cyclins
3: APC/C are separate regulatory proteins that initiate (metaphase--->anaphase) transitions during mitosis!
1)What kinase is responsible for inactivating the Cdk-cyclin complex and how does it do this?
B: How could we reverse this inactivation?
2) After cyclin binds to Cdk, how is the [Cdk-cyclin] complex activated as a group?
[Wee1 ] Kinase INACTIVATES Cdk-cyclin by phosphorylating 2 closely spaced sites above the 1st active site.
B: Cdc25 phosphatase has the ability to remove these inhibitory phosphates and reactivate Cdk-cyclin complex
2) CAK enzyme places FIRST activating phosphate on (Ser/Thr AA residues) of the
What happens when the Cdc25 ______ is ELEVATED?
Cdc25 PHOSPHATASE removes inhibitory phosphate pair from [Cdk-cyclin] complex-->reactivation. Reactivating too many [Cdk-cyclin] will lead to accelerated cell cycle stimulation
What is basically the step-wise process of regulating Cdk and cyclins? 
1st-cyclin binds to Cdk to activate Cdk= [Cdk-cyclin]
2nd- CAK enzyme phosphorylates Ser/Thr AA residues on the [Cdk-cyclin] complex-->ACTIVATE [Cdk-cyclin]
3rd- [Wee1 Kinase] adds 2 inhibitory phosphates to 2 close sites above active site-->INACTIVATION
4th- Cdc25 phosphatase removes inhibitory phosphates--------->REactivation of [Cdk-cyclin]
Describe Full Process of activating M-Cdk
1: As M-cyclin levels rise, M-cyclin binds to Cdk I =
2: activating phosphate then placed on [Cdk-Mcyclin] by CAK, followed w/inhibitory phosphate pair placed close to activation site by [Wee1 Kinase]
3: Resulting inactive [Cdk-Mcyclin] complex is then REactivated AT END OF G2 by Cdc25 phosphatase which removes inhibitory phosphate pair
4: now REactivated [Cdk-Mcyclin] is able to inhibit Wee1 Kinase AND is further stimulated by positive feedback from its other activated brothers
Ubiquitin Ligase Complex that promotes DEGRADATION of G1/S cyclin = STOPS CELL CYCLE PROGRESSION
1)What is Rb (____ _____)?
2)What is E2F
3)How would you INactivate Rb and what is the result?
1) Rb (Retinol Blastoma) susceptibility factor is a pocket binding protein that binds/inactivates E2F=NO S-PHASE
2) E2F upregulates S-phase genes--> G1/S-cyclin &S-cyclin production
3)When G1-Cdk comes and PHOSphorylate/INactivate Rb, Rb releases E2F --> E2F starts up S-Phase
When is Rb phosphorylated/_____[active/INactive]
Rb is PHOSphorylated/INactive during the G1------>S phase transition. (Allows E2F to start up s-phase stuff)
When is Rb DePhosphorylated/_____[active/INactive]
Rb is DePhosphorylated/ACTIVE during M----->G1 phase transition (You don't want E2F doing crazi S-phase stuff during Mitosis)
How do viruses cause upregulation in S-genes?
VP (viral proteins) OUT compete E2F tx factor for its binding pocket in the Rb protein and thus allow E2F to freely roam and overactivate [E2F element S-gene]!--->cell proliferation/CANCER
How does p53 assist in preventing cancer? 
2) This protein is effectively known as .....
*[G1] Damaged DNA activates protein kinases that phosphorylate p53(this DISbounds it from Mdm2 and activates p53!). --->
**p53 accumulates in high levels and stimulate tx of [CK1/p21/waf1] and also binds to/INactivates
[G1/S Cdk-cyclins] =arresting cell in G1-------->
****This allows time for cell to get it's act together/prevent cancer
2)p53 = "GUARDIAN OF THE GENOME"
2)What is an "alternative" process that occurs to this protein after DNA damage?
Binding Protein that BINDS to UNphosphorylated/INactive p53 and promotes their ubiquitylation/ destruction
2) Alternatively DNA damage also induces either Mdm2 phosphorylation OR decrease Mdm2 production------>will INC p53 levels as a result
1) [Ck1/p21/waf1] ?
2) What activates this?
1) Cyclin-Kinase inhibitor with 3 names lol! It STOPS cell cycle from proceeding -->gives cell enough time to repair before moving on after DNA damage in G1
2) [Ck1/p21/waf1] is activated by high levels of activated/phosphorylated p53