Cell Cycle Week 5 Holy Flashcards
Prophase-
first step of M phase or mitosis
- Replicated chromosomes condense
- mitotic spindle assemble between the two centromeres
first step of M phase or mitosis
- Replicated chromosomes condense
- mitotic spindle assemble between the two centromeres
Prophase
Prometaphase-
second step of mitosis
- nuclear envelope dissociates - chromosomes attach to spindle microtubules via kinetochores
second step of mitosis
- nuclear envelope dissociates - chromosomes attach to spindle microtubules via kinetochores
Prometaphase
Metaphase-
third step of mitosis
-chromosomes aligned at the equator of the cell
third step of mitosis
-chromosomes aligned at the equator of the cell
Metaphase
Anaphase-
fourth step of mitosis
- sister chromatids separate - kinetochore microtubules get shorter
fourth step of mitosis
- sister chromatids separate - kinetochore microtubules get shorter
Anaphase
Telophase-
fifth step of mitosis
- daughter chromosomes arrive at poles and decondense - new nuclear envelope begins to form - contractile ring forms around center of cell in preparation for cytokinesis
fifth step of mitosis
- daughter chromosomes arrive at poles and decondense - new nuclear envelope begins to form - contractile ring forms around center of cell in preparation for cytokinesis
Telophase
Cytokenesis-
contractile ring made of actin and myosin filaments pinches the cell in two creating two daughter cells
contractile ring made of actin and myosin filaments pinches the cell in two creating two daughter cells
Cytokenesis
Rho proteins-
small G proteins that stimulate actin polymerization; important in formation of contractile ring during telophase and cytokinesis
small G proteins that stimulate actin polymerization; important in formation of contractile ring during telophase and cytokinesis
Rho proteins
Cohesins-
multi protein complexes that help keep replicated chromosome pairs (daughter chromatids) together until it is time to separate them during, help prevent premature separation and aneuploidy
multi protein complexes that help keep replicated chromosome pairs (daughter chromatids) together until it is time to separate them during, help prevent premature separation and aneuploidy
Cohesins
Condensins-
multi protein complexes related to cohesins but are involved in the tight packaging of chromatin in mitosis
multi protein complexes related to cohesins but are involved in the tight packaging of chromatin in mitosis
Condensins
Kinetochore-
complex of protein that assembles on centromeric DNA, made up of centromeric heterochromatin, histone H3 variant called CENP-A. Identifies the location for kinetochore formation.
complex of protein that assembles on centromeric DNA, made up of centromeric heterochromatin, histone H3 variant called CENP-A. Identifies the location for kinetochore formation.
Kinetochore
CENP-A-
histone H3 variant located on the centromeric heterochromatin; identifies location for assembly of kinetochores
histone H3 variant located on the centromeric heterochromatin; identifies location for assembly of kinetochores
CENP-A
Kinetochores-
interact with microtubule of the spindle apparatus for separation of daughter chromatids; have signaling function as metaphase checkpoints
interact with microtubule of the spindle apparatus for separation of daughter chromatids; have signaling function as metaphase checkpoints
Kinetochores
Kinetochore microtubules-
pull daughter chromosomes apart at kinetochores
pull daughter chromosomes apart at kinetochores
Kinetochore microtubules
Interpolar microtubules-
push chromosomes away from poles to align during formation of metaphase plate; also push against eachother to elongate the spindle in late anaphasae
push chromosomes away from poles to align during formation of metaphase plate; also push against eachother to elongate the spindle in late anaphasae
Interpolar microtubules
Astral microtubules-
push chromosomes away from poles during formation of metaphase plate
push chromosomes away from poles during formation of metaphase plate
Astral microtublues
Contractile ring-
formed by contractile fibers of actin and myosin which are controlled by Rho; pinches of two cells during cytokinesis
formed by contractile fibers of actin and myosin which are controlled by Rho; pinches of two cells during cytokinesis
Contractile ring
CDK-
cyclin dependent kinase, the catalytic subunit of the cell cycle
cyclin dependent kinase, the catalytic subunit of the cell cycle
CDK
Cyclin-
the regulatory subunit of the cell cycle
the regulatory subunit of the cell cycle
Cyclin
CKIs-
cyclin dependent kinase inhibitors; two families, CIP/KIP (p21,p27), and Ink4a (p15, p16
cyclin dependent kinase inhibitors; two families, CIP/KIP (p21,p27), and Ink4a (p15, p16
CKIs
CIP/KIP (p21, p27)-
CKIs that bind cyclin-CDK complexes; upregulated by p53 in response to DNA damage
CKIs that bind cyclin-CDK complexes; upregulated by p53 in response to DNA damage
CIP/KIP (p21, p27)
Ink4a (p15, p16)-
bind to CDK subunits and prevent cyclin association, upregulated by environmental signaling
bind to CDK subunits and prevent cyclin association, upregulated by environmental signaling
Ink4a (p15, p16)
Cyclin D, CDK 4 or 6 (which phase?)-
associated with G1
Cyclin B, CDK 1 (which phase?)-
associated with M phase
CAK-
phosphorylates active site of CDK
phosphorylates active site of CDK
CAK
Wee1 kinase-
phosphorylates deactivation site of CDK; inhibited by active M-Cdk→positive feedback for continuation of M phase
phosphorylates deactivation site of CDK; inhibited by active M-Cdk→positive feedback for continuation of M phase
Wee1 kinase
Cdc-25-
removes phosphate added to CDK by Wee1, activates M-Cdk which activates more Cdc-25 through positive feedback
removes phosphate added to CDK by Wee1, activates M-Cdk which activates more Cdc-25 through positive feedback
Cdc-25
Mitogen growth factor-
activates Ras G protein on plasma membrane to move cell from G0 to G1
activates Ras G protein on plasma membrane to move cell from G0 to G1
Mitogen growth factor
Ras-
activated by mitogen growth factor, Ras activates MAP kinase cascade
activated by mitogen growth factor, activates MAP kinase cascade:
Ras
MAP kinase-
Activated by MAP-kinase-kinase-kinase→MAP-kinase-kinase, eventually crosses into nucleus and activates transcription factors by phosphorylating them
Rb-
retinal blastoma protein, an important cancer suppressor, acts by binding to EF2 which is a transcription factor in cell division
EF2-
transcription factor in cell division which can be inhibited by Rb
ORCs, what are they, what phase?
- origin of replication complexes; (G1)
Cyclins E and A- what do they do? When do we see them?
produced towards the end of G1, activate CDK2
CDK2- function?
recruits preinitiation complex proteins (Cdc6, Cdt1) to ORCs
Cdc6- function and fate?
preinitiation complex protein destroyed by Cdk activity after triggering of DNA synthesis so DNA is not replicated more than one in a cycle
APC- how’s it activated? what are its two main jobs?
Anaphase Promoting Complex; activated by M-Cdk, it inactivates securin which is an inhibitor of separase which promaotes the destruction of cohesin and allows attached chromatids to separate; also destroys CDK activity, ending M phase and initiating cytokenesis
Securin- what does it do?
inhibits separase
Seperase- what does it do?
promotes destruction of cohesin and subsequently the separation of attached chromatids
Cyclin B-
ubiquinated by APC for destruction, abolishes CDK activity ending M phase
ubiquinated by APC for destruction, abolishes CDK activity ending M phase
Cyclin B
G1 checkpoint requirements-
if extracellular environment is favorable→ G1/S cyclin and Cdk synthesis and progression into S phase
if extracellular environment is favorable→ G1/S cyclin and Cdk synthesis and progression into S phase is called:
G1 checkpoint
G2/M checkpoint-
makes sure environment is favorable and all DNA is replicated for transition into M phase
M phase checkpoint-
ATM/ATR kinases activate if the detect DNA damage; they in turn activate Chk1/Chk2 kinases which phosphorylate p53; p53 is a transcription factor for CKI p21 which blocks Cdk activity and halts cell cycle for attempted DNA repair
ATM/ATR kinases activate if the detect DNA damage; they in turn activate Chk1/Chk2 kinases which phosphorylate p53; p53 is a transcription factor for CKI p21 which blocks Cdk activity and halts cell cycle for attempted DNA repair
M phase checkpoint
ATM/ATR kinases-
sense DNA damage during M phase checkpoint and activate Chk1/Chk2 kinases if damage exists
sense DNA damage during M phase checkpoint and activate Chk1/Chk2 kinases if damage exists
ATM/ATR kinase
Chk1/Chk2 kinases-
activated by ATM/ATR when DNA damage is present in M phase; the phosphorylate and activate p53
activated by ATM/ATR when DNA damage is present in M phase; the phosphorylate and activate p53:
Chk1/Chk2 kinases
What is the function of p53-
critically important protein activated by Chk1/Chk2 and upregulated when DNA damage is present in M phase. p53 functions as a transcription factor for CKI 21 which blocks Cdk activity and halts cell cycle
critically important protein activated by Chk1/Chk2 and upregulated when DNA damage is present in M phase. functions as a transcription factor for CKI 21 which blocks Cdk activity and halts cell cycle
p53
Spindle checkpoint-
unattached kinetochores activate Bub and MAD2 proteins which inhibit activation of APC thereby blocking anaphase initiation and Cdk destruction; this keeps the cell in pro/metaphase until all kinetochores can bind to microtubules and become aligned in metaphase plate
unattached kinetochores activate Bub and MAD2 proteins which inhibit activation of APC thereby blocking anaphase initiation and Cdk destruction; this keeps the cell in pro/metaphase until all kinetochores can bind to microtubules and become aligned in metaphase plate
Spindle checkpoint
Bub-
protein activated by unattached kinetochores that inhibits APC and prevents progression into anaphase until all kinetochores are attached to microtubules
MAD2-
protein activated by unattached kinetochores that inhibits APC and prevents progression into anaphase until all kinetochores are attached to microtubules
Oncogenes-
mutated genes whose presence can stimulate the development of cancer
Tumor suppressor genes-
normal genes whose ABSENCE can lead to cancer