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Final Flashcards

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1
Q

Overview of Cell Cycle

A

●four coordinated processes that leads to cellular duplication: reproduction
●G1, S, G2, M

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2
Q

S phase

A

●synthesis of DNA
●DNA is duplicated

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3
Q

M Phase

A

●mitosis
●chromosomes segregate into the daughter cells

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4
Q

G1 phase

A

●Gap phase 1
●cell physically grows
●if in the proper environmental conditions are met -> cells enters S phase -> commitment to reproduction
●membrane grows, cytoskeleton, more proteins

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5
Q

G2 phase

A

●Gap phase 2
●cell continues to grow, proteins and organelles are made
●preparation to mitosis -> cell division

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6
Q

Gap 1

A

●environmental conditions -> signal transduction pathways
●mTOR is hyperactivated

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7
Q

Gap 2

A

●cellular conditions
●checkpoint pathways (check condition of DNA)

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8
Q

G1/S checkpoint

A

●cell commits to cell duplication
●checking for environmental favorable conditions to replicate

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9
Q

G2/M checkpoint

A

●mitotic entry
●Checking for DNA errors

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10
Q

M/G1 checkpoint

A

●metaphase to anaphase transition
●stimulation of chromosomes separations and cytokinesis
●checking for correct chromosomes alignment

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11
Q

G0

A

●cells that are fully developed
●no replication or preparing to divide

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12
Q

Cyclin binding activates Cdk

A

●cyclin-dependent kinases govern cell cycle progression
●Cdks are not active until cyclins bind to them
●Cdks are constantly expressed during cell cycle
●cyclin induce conformational change of Cdk
●Cdk phosphorylates other proteins
●formation of Cdk-cyclin complexes

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13
Q

Cyclins throughout cell cycle

A

●cyclins expression changes throughout cell cycle
●fluctuates
●when cyclins bind to Cdks activate complex
●complexes phosphorylate target proteins that govern cell cycle progression

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14
Q

how is cyclin expression changed throughout cell cycle?

A

●regulate cyclin
●affect TF- controlled by signaling pathways
●Degradation

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15
Q

increase and decrease of cyclin

A

●G1/S cyclin increase during G1 until peaks
●at peak S-cyclin begins to start cell cycle
●S-cyclin until G2 where M-cyclin begins to increase into M
●M-cyclin reaches peak at down regulation of S-cyclin

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16
Q

Turning off Cdk/Cyclin activity: CKI

A

●CKI binding switches off Cdk/Cyclin complex
●Control activities of G1/S complexes and early S complexes
●CKI binds to both Cdk and Cyclin distorting their activities

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17
Q

Turning off Cdk/cyclin activity: APC Anaphase promoting complex

A

●promote cytokinesis
●APC is active mid-mitosis and G1
●APC target S and M cyclins
●APC is member of ubiquitin family
●tags protein with ubiquitin to take to proteosome
●APC promotes destruction of securin (chromosome separation)
●Targets S phase cyclin
●Activation of APC depends on CDC20 and Cdh1 -> ubiquitin= targeting cyclins for proteosome

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18
Q

Turning off Cdk/cyclin activity: SCF

A

●SCF belongs to ubiquitin Family
●target CKI promoting S phase and DNA synthesis
●Target S phase cyclin

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19
Q

Turning off Cdk/cyclin activity: inhibitory phosphorylation

A

●activity of Cdc25 promotes activation of Cdk-M cyclins -> mitosis
●Wee1 phosphorylates Cdk -> inactive
●Cdc25 dephosphorylates Cdk -> activates
●dephosphorylation of Cdk-M cyclins promotes entry in mitosis

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20
Q

Activation of Cdk-M complex via positive feedback

A

●accumulation of M cyclins during G2
●inhibitory phosphorylation by Wee1
●activation of Cdk-M by phosphatase Cdc25
●activation of Cdk-M promotes positive feedback: Cdk-M complex inhibits phosphatase PP2A-B55 promoting increasing of CDC25 phosphorylated species, Cdk-M complex inhibits phosphatase PP2A-B55 promoting inactivity of Wee1
●Cdk-M complex positive feedback: inhibition of inhibitor Wee1 and activation of activator Cdc25
●Cdc25 without phosphate=inactive
●Wee1 with phosphate=inactive

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21
Q

Mechanisms for downregulation of CDK-cyclin

A

●degradation of cyclins
●inhibitory phosphorylation of Cdk
●CKI binding- turns it off

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22
Q

S Phase: initiation of DNA synthesis

A

●binding to MCM helicase at origin of replication during late G1/S phase
●replication happens only at origins pre-loaded with helicase
●origins are recognized by ORC (origin recognition complex)
●once in S phase can’t go back

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23
Q

S phase: activation of helicase

A

●helicase activated in S phase -> formation of replication bubble
●CDK/S complexes trigger activation of helicases (phosphorylation?)
●once activated, replication of DNA starts
●Once origin is used, it can not be reloaded with helicase until the next cycle (ensure DNA is only replicated once)

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24
Q

Activation and control of replication

Study These Flashcards
A

●CDK/S complexes stimulate formation of Cdc25/Gins/MCM complex
●Cdc25 and Gins are accessory proteins involved in positioning helicase and unwinding dsDNA
●MCM is helicase
●CdK/S complexes also deactivate proteins involved with recruitment of helicase to origins -> this avoids recruitment of more helicases (Origins phosphorylation)
●DDK is a kinase that activates helicase (not dependent on cyclin)

25
Cohesin
●keeps together sister chromatids during S and G2 phase ●is a complex of four subunits ●has hinge domain, coiled-coil domain (SMC3 and SMC1), ATPase domain, and Scc1 ●ATP is needed to open and close complex, important for loading and unloading DNA ●used until after M
26
Stages of Mitosis
●interphase ●prophase ●prometaphase ●metaphase ●anaphase ●telephase ●cytokinesis ●interphase
27
Cytoskeleton in mitosis
●guides movement in daughter cells
28
Prophase
●chromosomes condense (two copies of each chromosomes) ●two replicated chromosomes move apart ●centrosome are center of nucleation ●mitotic spindle start to assemble ●centrosomes for microtubule
29
Prometaphase
●Chromosomes attach to spindle at kinetochore (attach chromosomes) -> chromosomes start the movement to metaphase plate ●microtubules elongate ●nuclear envelope breaks up ●before alignment, nuclear membrane breaks up
30
Metaphase
●chromosomes align to metaphase plate, midway between spindle poles ●chromosomes perfectly align ●establishment of polarity
31
Anaphase
●sister chromatids separate ●each chromosomes is pulled towards spindle poles ●microtubules from kinetochores shorten by depolymerization ●spindle poles move further apart ●indent starts to form in cell membrane
32
Telophase
●chromosomes reach spindle poles ●chromosomes decondense and new nuclear envelope forms around decondensed DNA completing formation of two nuclei ●constriction ring starts to form ●create nucleus in daughter cell ●chromosomes condense to move around easier and separate
33
Cytokinesis
●cytoplasm is divided in two by contractile ring made of myosin and actin ●ring clips the cell to create two daughter cells ●end of mitosis
34
1 Mitosis regulatory mechanisms
●increase Cdk/M activity at late G2 phase trigger early mitosis phases (prophase, prometaphase, metaphase) ●spindle pole body separation, spindle formation, synthesis of Cdc20 ●cdc20 necessary to work with APC for ubiquitination
35
2 mitosis regulatory mechanisms
●APC triggers destruction of securin, promoting sister chromatids separation ●moreover, APC in complex with Cdc20 targets destruction of early mitotic cyclins ●CDK-M -> synthesis of cdc20, APC phosphorylation, inhibition of cytokinesis ●because early cyclin trigger beginning of phases of mitosis, don't need spindle or chromosomes in middle, caused by APC
36
Cdc20 directs Clb3-6 degradation
●Cdc20-APC complex targets cyclin for ubiquitination ●Cdk reused ●cyclin to proteasome for degradation ●targets activated by Cdk/M are not phosphorylated anymore (cuz there is no more cyclin) ●exit from mitosis
37
APC-Cdc20 controls chromosomes separation
●Cdk/M complexes activated spindle formation ●APC/Cdc20 targets securin to degradation ●destruction of securin leads to release of separase (activated) ●separase cleaves cohesin promoting chromosomes separation
38
Control of division and size
●size of organism (uni or multicellular) depends on total cell mass ●cell mass depends on number of cells and size of cells ●number of cells depends on number of cell divisions ●-> cell cycle
39
Mitogens stimulates cell division
●microorganisms divide very fast and when nutrients are available (sufficient food) ●multicellular organisms cell division is stimulated by mitogens (PDGF- platelet derived growth factors, EGF- epidermal growth factors, erythropoietin- red blood cells) ●inhibitory factors that stimulate growth arrest (stop in G1, doesn't commit to S)
40
G0 phase
●inhibition of CdKs and cell cycle mechanisms ●G1 is longest phase of cell cycle ●S-G2 and M are faster ●cell not dividing stay in G0 (entering G0 is commitment)
41
Mitogens
●stimulate CdKs/G1 and CdKs/S activities
42
Mitogen cascade
●extracellular signal can regulate cell cycle progression ●mitogens activate a signaling cascade to promote synthesis of transcription regulators, such as MYC ●MYC promotes the cell cycle entry via different mechanisms: G1 cyclins, genes involved in cell growth ●immediate response genes: genes that are rapidly activated upon stimuli
43
Rb cycle
●MYC-> delayed response genes -> G1CdK-> Rb (E2F) ●Rb retinoblastoma protein binds to E2F (regulatory TF) (this prevents the binding of E2F to DNA) ●CdK/G1 complex inhibits Rb via phosphorylation (inhibition of Rb releases E2F)(E2F now promotes transcription of S phase genes) ●S phase genes: S cyclins, genes involved in DNA synthesis and chromosomes assembly ●increasing the synthesis of cyclins leads to increase of CdKs/cyclins complexes activity
44
E2F positive feedback
●E2F promotes the transcription of S cyclins ●CdK/S complex reinforces activation of S-phase genes transcription via release of E2F ●some S-phase genes activate themselves
45
Why does mutating Rb cause excessive growth?
●overactivation of E2F -> enter S phase uncontrollably ●will also enter w/ damage cuz no more checkpoint
46
Rb eye cancer
●Rare but treatable, also no hereditary form ●homozygotic mutation in Rb gene ●mutate Rb causes excessive retinal cell growth ●partially attenuated by CKIs or by Rb-related proteins
46
Intracellular signals that regulate cell cycle
●intracellular signal= DNA damage ●DNA damage recognized in G1 phase (Kinases ATM and ATR can associate with DNA damage) (recognize damage) ●P53 (gene regulatory protein, TF), when activated promotes the transcription of p21(CKI) (target S cyclin) ●DNA damage also recognized in G2 phase (homologous recombination)
47
What happens if p53 is mutated?
●p53= tumor suppressor protein ●leads to uncontrolled entry in S-phase thus cell division -> tumor mass ●mutation in P53 can be vast because the cell can divide also in presence of DNA damage (lead to reproduction of dna damage) ●P53 frequently mutated in aggressive types of cancer
48
Cell growth is fundamental for cell survival
●without cell growth, cell would become smaller at each division -> loss of mass ●cell proliferation requires an increase in cellular mass ●during cell cycle, a cell grows in G1 and G2 phase ●microbes divide when they have food, eukaryotes have mitogens, growth factors, and nutrients
49
What does mTOR respond to
●nutrients and mitogens
50
Apoptosis: Cell suicide
●programmed cell death ●very regulated ●important in multicellular organisms and cell development ●damaged (eg. DNA) and very stressed cells can undergo apoptosis ●apoptosis is different than necrosis (cell membrane is destroyed)
51
Apoptosis more
●dramatic changes: cytoskeleton collapsing, nuclear membrane, and chromosomes disassembling ●formation of protrusions -> bleeping ●apoptotic bodies, membrane-enclosed vesicles that are engulfed by other cells, such as lymphocytes ●sometimes apoptosis is balanced by cell growth and division -> homeostasis
52
Apoptosis: molecular regulators
●Caspase are proteases (enzyme that breaks down proteins by targeting peptide bonds). Cysteine in their active site and they target aspartic acid on target protein ●Procaspases (precursor) exists in cytoplasm. Activated during apoptosis ●procaspase -> caspase (only activated when needed) ●two kind of apoptotic caspases: initiator and executioner caspases
53
Extrinsic Pathway
●need extracellular signal ●death activators (FAS receptors) on cell surface (sometimes death receptors form trimers when the ligand binds to them) ●binding of ligand exposed the death domain (intracellular domain, in picture of FADD), receptors are now activated ●procaspases bind to receptor ●procaspases is cleaved and initiator caspase is not active ●caspase now activate executioner caspase ●executioner caspase cleaves cellular proteins such as actin, microtubules, and other proteins -> apoptosis ●DISC complex mase of death receptor, adaptor and procaspase ●when DISC complex is formed, the procaspase is turned into initiator caspase by proteolytic cleavage ●NO DEGRADATION
54
Caspase with DNA
●cant cut DNA cuz only cuts peptide bonds ●cut histones and activate other proteins
55
Activation of Procaspase
●initiator caspase is inactive ●two important cleave sites: between adaptor binding domain and protease domain, and in protease domain ●cross-cleavage between caspases leads to release of an active caspase dimer form DISC ●apoptotic signal -> cleave both sites -> large subunit and small subunit rearrange (change conformation)
56
Apoptosis: intrinsic pathway
●activated from intracellular signals (DNA damage - signal arrives to mitochondria) ●Cytochrome C when released in cytoplasm binds to an adaptor protein called APAF1 ●APAF1 binds oxidized ATP and forms a very large complex called Apoptosome ●Apoptosome activates initiator caspase also via dimerization ●initiator caspase activates effector caspase
57
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Adv Cell Bio (4 decks)

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