Cell Cycle (Dr. Pfeffer) Flashcards
What is the basis of cell cycle control?
cyclically activated protein kinases
What is cell cycle control?
a series of counter balances…
- synthesis and degrdation
- phosphorylation and dephosphorylation
Who were the first to characterize cell cycle regulation in different organisms? (this was in red on the ppt…)
Hartwell, Hunt and Nurse (in the ’70s and ’80s)
Microtubule and microfilament disruption will cause the cell cycle to arrest at ___ phase?
M
If DNA replication is disrupted at what phase will the cell cycle arrest?
S
What agents disrupt microtubule function?
vincristine
vinblastine
taxol
colchicine
*arrests cell at M phase
What agents disrupt microfilament structure?
cytochalastin
*arrests cell late in M phase bc this blocks cytokinesis
What is the longest phase of the cell cycle?
G1
What phases of the cell cycle is the chromosome state 4n?
Late S, G2, early M
When will stable cells begin to divide?
When they receive a signal
When will permanent cells begin to divide?
they don’t divide (for the most part)
______ function to ensure correct cycling.
Checkpoints
What is “checked” at the G1 checkpoint?
Is the cell big enough?
Is the enviro right?
Is DNA damaged?
What is “checked” at the G2 checkpoint?
Is all the DNA replicated?
Is the cell big enough?
Describe the Rao and Johnson nuclear fusion experiments? (4 tests)
Nuclei in various phases of the cell cycle we combined to see if the different phases had factors assc with it that influence cells to enter into certain parts of the cell cycle
- S + G1 –> S
(S cell “releases” factors induce G1 to proceed into S) - S + G2 –> nothing
(G2 is resistant to factors from S phase cell) - G1 + G2 –> nothing
(G1 and G2 do not have factors that influence each other) - interphase + M –> M
(M phase has factors that induce all other cells to enter into M phase)
What happens to cells that are not read to transit into the S phase from G1?
go into G0 phase
What happens to cells in G1 that are under stress?
apoptosis
What happens in S phase?
DNA replication and sythsis of DNA pol and histones
What happens in G2 phase?
synthesis of proteins needed for mitosis
What happens in M phase?
mitosis
What is the Hayflick number?
proliferation potential od cells (as we age, out hayflick number decreases (inverse relationship))
What is progeria?
pre-mature aging disease
What is senescence?
cells are alive but are not dividing (occurs when cells have reached their proliferation potential
The time spent in ____ phase is highly variable (meaning in many different studies, researchers found wide ranges of time spent in this phase relative to other phases)
G1
What is MPF?
maturation promoting factor
or
cyclin B + Cdc2 kinase
What happens to a cell arrested in G2 and then has MPF added to it?
it enters in M phase
What happens to a cell arrested in G2 and then has progesterone added to it?
it enters into M phase
MPF promotes ____ in somatic cells
mitosis
MPF activity oscillates in assc with _____
cyclin conc
T or F: MPF concentration oscillates throughout the cell cycle
F: the conc on MPF is constant
Why does cell division not constantly occurring?
cyclin levels are not constant. M phase occurs only when cyclin is present
MPF =
cyclin B + Cdc2 kinase
WIll a larger or smaller yeast “bud” enter into S phase faster?
bigger bud bc the smaller one must grow in order to move past the G1 checkpoint
What effect does Wee1 gene have on MPF?
inhibits it
What effects does Cdc25 have on MPF?
activates it
What is the result of excess Cdc25 and deficient Wee1?
small cells that spend less time in G2
What is the result of deficient Cdc25 and excess Wee1?
elongated cells that spend more time in G2
Describe active MPF.
Y15 is NOT phosphorylates and T161 is phosphorylated. This allows for the substrate binding site to be exposed
Is completely dephosphorylated MPF active or inactive?
inactive
What is p27? What is its role in the cell cycle?
it bind to ACTIVE cyclin-Cdk complex (MPF) to inactivate it
Mitotic Cdk is made during __ phase but kept inactive until ___ phase
G2; M
What is the role of SCF?
when active, it phosphorylates p27 (Cdk inhibitor) to tag it for ubiquination/degradation by proteosome
*regulator of proteolysis
What is the role of APC? (anaphase promoting complex)
when APC is bound by Cdc20 it is active –>
active APC tags Cyclin M-Cdk complex for ubiquination/degradation
If you have defective or deficient SCF, what is the effect in the cell cycle?
Cdk is inhibited more frequently bc there is more p27 (or Cdk inhibitor)
How does SCF have to be altered to lead to unregulated cell proliferation?
if SCF is constitutively active, Cdk inhibitor (p27) is constantly being degraded –> Cdks are constantly active –> cell cycle on
***this was not from the notes, this is me trying to come up with things they may make up come up with… so I’m probably wrong somewhere in my reasoning
How does APC have to be altered to lead to unregulated cell proliferation?
if APC mutated so that it can cannot be activated by Cdk20 binding –> Cdk-Cyclin M is not degraded –> can turn on cell cycle
If active APC cannot bind Cdk-Cyclin M complex –> cell cycle on bc Cdk-Cyclin M is not degraded
***this was not from the notes, this is me trying to come up with things they may make up come up with… so I’m probably wrong somewhere in my reasoning
At what phase of mitosis in APC active? inactive?
active during late anaphase
inactive during prophase (When cyclin B is made)
When in the cell cycle is MPF active?
G2 checkpoint to induce M phase
When S cyclin is present what occurs?
cell proceeds into S phase
When M cyclin is present what occurs?
cell proceeds into M phase
How are cyclins regulated?
phosphorylation, inhibitors (p53, p27, etc), conc of cyclins (Tx or proteolysis=APC)
