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MCBG Exam 3 > Cell Cycle (I, II & III) > Flashcards

Cell Cycle (I, II & III) Flashcards

1
Q

What are the major phases of the cell cycle?

A 
Mitosis (M)
Gap phases (G1 and G2)
Synthesis phase (S)

Order: M–>G1–>S–>G2–>M ….. etc.

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2
Q

What are the two main components of M phase?

A

Mitosis: nuclear division
Cytokinesis: cytoplasmic division

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3
Q

What is interphase?

A

The period between subsequent M phases

Made up of G1, S and G2

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4
Q

What happens in the Go stage?

A

The Go stage is outside of the cell cycle
The cell cycle machinery is lost and cells are either senescent (permanently out of cycle), or quiescent (temporarily out of cycle)

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5
Q

What are the 3 major checkpoints in the cell cycle?

A

G1 checkpoint: is environment favorable for S phase?
G2 checkpoint: is environment favorable for mitosis? Is DNA replication properly completed?
Metaphase checkpoint: Are all chromosomes attached to spindle?

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6
Q

What is the cell cycle control system?

A

A complex network of regulatory proteins that ensures events are properly timed and occur in the correct order

Feedback in order to regulate the cell cycle

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7
Q

The concentration of what class of proteins regulates the cell cycle?

A

Accumulation of cyclins regulates the cell cycle

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8
Q

Describe the active form of cyclin-dependent kinase

A

Cdk is active when it is bound to cyclins and phosphorylated in the correct location
Once active, it can activate other proteins via phosphorylation

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9
Q

Describe the concentration of Cdk’s throughout the cell cycle

A

Cdk’s are not degraded during the cell cycle. The concentration of cyclins determines which Cdk’s are active when

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10
Q

Describe the phosphorylation of Cdk and its impact on Cdk activity

A
  • Cdk has an activating phosphate site as well as inactivating phosphate sites.
  • CAK’s activate Cdk by phosphorylating the activating site
    If any inhibitory sites are phosphorylated, Cdk will be inactive
  • Cdc25 is an activating phosphatase that removes inhibitory phosphate groups
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11
Q

What is the APC?

A

Anaphase Promoting Complex

- Exit from mitosis by degradation of M-cyclin

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12
Q

Describe what happens to M-Cdk during mitosis

A

The accumulation of M-cyclin triggers activation of M-Cdk by M-CAKs and M-Cdc25
Near the end of mitosis, the APC degrades M-cyclin, leading to the exit from mitosis

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13
Q

What complex is analogous to the APC, but for S phase?

A

SCF is analogous to the APC

SCF degrades G1/S cyclins

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14
Q

What is the function of Rb proteins?

A

Rb proteins regulate cell proliferation

1) When de-phosphorylated, Rb sequesters E2F
2) When Rb is phosphorylated, it releases E2F which leads to activation of genes related to S phase
3) S-cyclin-Cdk complex active and S phase begins

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15
Q

How can viral proteins impact the regulation of the cell cycle?

A

Viral particles can compete with E2F for binding to Rb proteins. This results in excess E2F being active, causing up-regulation of the cell cycle, continues cell replication

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16
Q

What is p53?

A

“Guardian of the genome”
A tumor suppressor gene that is crucial for regulating the cell cycle entry into the S-phase

50% of cancers have a loss of function of p53

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17
Q

What proteins does p53 act on in order to give cell time to repair damage before entering the S phase?

A

p53 activates p21 (waf1/CIP) which then binds to G1/S-Cdk’s and inhibits their activity
Inhibited G1/S Cdk’s cannot phophorylate Rb to release E2F, thus preventing entry into the cell cycle

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18
Q

How is the concentration of p53 regulated?

A

The concentration of p53 is regulated via interaction with Mdm2, which is constantly leading to degradation of p53 in the lysosome.

The degradation rate is variable depending on the cell cycle stage

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19
Q

How is p53 modified when DNA damage occurs?

A

p53 is phosphorylated following DNA damage

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20
Q

What are the major steps in mitosis?

A

Prophase, prometaphase, metaphase, anaphase, telophase, cytokinesis

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21
Q

What major events occur in prophase?

A

Sister chromatids condense

Mitotic spindle assembles

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22
Q

What major events occur in prometaphase?

A

Nuclear envelope breakdown

Chromosomes attach to spindle microtubules

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23
Q

What major events occur in metaphase?

A

Chromosomes align at equator

Kinetochore microtubules attach sister chromatids to opposite poles

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24
Q

What major events occur in anaphase?

A

Sister chromatids separate
Kinetochore microtubules shorten
Spindle poles move apart

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25
Q

What major events occur in telophase?

A

Chromosomes arrive at poles
New nuclear envelope assembles
Contractile ring forms

26
Q

What is cytokinesis?

A

Cytoplasmic division mediated by the contractile actin/myosin ring
Produces 2 separate daughter cells

27
Q

Describe the structure of the nuclear membrane

A

A square lattice of lamin intermediate filaments

28
Q

What structural modification of lamin causes nuclear envelope degradation?

A

Phosphorylation of lamins and nuclear pore proteins triggers the breakdown of the nuclear envelope

29
Q

Describe the reformation of the nuclear envelope

A

In late telophase, vesicles of nuclear membrane form around individual chromosomes, which then merge to form the whole nucleus

30
Q

When do centrosomes replicate?

A

During the S phase, at the same time as DNA replication

31
Q

What are the steps in centrosome replication?

A

The centrioles detach from each other and then duplicate, forming daughter centrioles from the two original centrioles.
Spindle fibers push the newly formed pair of centrosomes apart

32
Q

How does microtubule dynamic instability help with kinetochore attachment?

A

The instability of the microtubules causes rapid cycles of catastrophe and rescue. This increases the chance of kinetochore capture due to this “searching” motion

33
Q

How do Cyclin dependent kinases (Cdks) regulate dynamic instability?

A

Cdk’s inactivate MAPs by phosphorylation and activate kinesin by phosphorylation leading to a ten fold increase in dynamic instability

34
Q

What are the three classes of mitotic microtubules?

A

Astral
Kinetochore
Interpolar

35
Q

Describe the general structure of condensins and cohesin

A

2 Smc proteins (each a dimer), and 3 non-SMC subunits (CAPs) form a ring structure that can encircle loops of DNA

36
Q

How do the functions of condensin and cohesin differ?

A

Condensin promotes condensation of chromosomes

Cohesin joins sister chromatids together

37
Q

True or false: each chromosome has one alpha satellite DNA monomer that defines where the centromere will be

A

False. Centromeres are defined by the assembly of proteins and not solely by the DNA sequence.
There are alpha satellite DNA monomers in heterochromatin as well as in the centromere

38
Q

How do centromere specific histones attach to microtubules?

A

The CENPA histones bind to kinetochore proteins (complex of at least 12 proteins) which then can interact with the mitotic spindle

39
Q

What is the difference between anaphase A and anaphase B?

A

These are two simultaneous mechanisms by which chromatids move apart from each other
A: Kinetochore microtubules shorten by depolymerization, chromosomes move toward poles
B: Kinesins and dyneins move the centrosomes apart by pushing from midline and pulling from cortex

40
Q

What are the major substrates of Cdk1 mentioned in class?

A

Condensin, Nuclear lamin, Motor proteins, MAPs, Catastrophins, APC-cdc20

41
Q

Describe the molecular mechanism of the M-phase checkpoint

A

DNA Damage is recognized by kinases ATM/ATR resulting in cell cycle arrest before M-phase
Two different pathways:
1) ATM/ATR activates p53 by phosphorylation; p53 upregulates the CKI p21, which inhibits M-cdk and prevents entry into M-phase
2) ATM/ATR activates Chk1/Chk2 by phosphorylation; Chk proteins inactivate cdc25 by phosphorylation which prevents the inhibitory phosphate from being removed from cdk, entry into M-phase prevented

42
Q

What is APC and what does it do?

A

Anaphase promoting complex

Triggers entry into anaphase from metaphase by activating separase

43
Q

Describe the molecular events surrounding activation of APC

A

1) M-cdk phosphorylated cdc20
2) cdc20 binds to APC and activates it
3) APC-cdc20 promotes ubiquitination and degradation of securin and degradation of M-cdk
4) Securin releases active separase
5) Separase can degrade cohesin to allow chromatids to separate

44
Q

Describe the regulation of entry into anaphase from metaphase (Hint: APC, MCC interaction)

A

As long as unbound kinetochores exist, MAD2 will shuttle between its active and inactive state and cdc20 will be sequestered in the Mitotic Checkpoint Complex (MCC).

Once all kinetochores are bound, MAD2 loses its inhibitory function and allows MCC to dissociate from cdc20. Cdc20 is then phosphorylated by Cdk and APC is activated leading to anaphase

45
Q

What is the most common class of enzyme coupled receptor?

A

Receptor Tyrosine Kinases (RTKs)

46
Q

How are RTKs activated?

A

Dimerized ligands (mitogen/growth factor) bring two inactive RTKs close together by binding

The dimerized RTKs cross-phosphorylate each other to produce phosphorylated binding sites for other proteins

47
Q

Can a membrane bound molecule activate an RTK protein?

A

Yes. Mitogen molecules can be membrane bound. Cell-cell contact is required for RTK activation
example: Ephrins activating Eph receptors

48
Q

How are signals relayed downstream from activated RTKs?

A

Intracellular signaling proteins bind to phosphorylated tyrosines to activate multiple signaling pathways

49
Q

What is an SH2 domain?

A

Protein domain that can bind to phosphorylated tyrosines

50
Q

What are the two binding sites on SH2 domains?

A

One binds to the phosphorylated tyrosine
The second binds to amino acid side chains near the tyrosine

This produces highly specific binding

51
Q

Describe the structure of Src

A

Src is a cytosolic membrane bound protein kinase. It does not have a extracellular receptor, so it needs to complex with a receptor to be activated

52
Q

Describe the activation of Ras by an RTK

A

1) RTK is activated following ligand binding, cross-phosphorylation
2) GRB2 adaptor protein binds to phosphorylated tyrosines via SH2 domain
3) SH3 domains of GRB2 bind to polyproline helical structure of GEF
4) GEF activates Ras by exchanging GDP for GTP
5) Activated Ras will initiate the MAP kinase module

53
Q

Is Ras considered an oncogene or a tumor suppressor?

A

Ras is an oncogene. Constitutive expression leads to massive cell proliferation, cancer

54
Q

Describe the mitogen activated protein kinase cascade

A 
MAPK cascade
Ras-Raf-Mek-Erk
1) Ras interacts with MAP-KKK (Raf)
2) MAP-KKK phosphorylates MAP-KK (MEK)
3) MAP-KK phosphorylates MAP-K (ERK)
4) MAPK activates transcription factors leading to altered gene expression and protein activity
55
Q

What gene regulatory protein is activated by MAPK in order to enter into S phase?

A

Myc

Myc activates the synthesis of G1 cyclins leading to active G1-cdk

56
Q

What is the main function of G1-cdk?

A

To activate E2F by phosphorylating Rb to release E2F

Causes transition into S phase

57
Q

Do tumor suppressor genes act recessively or dominantly?

A

TSGs act in a recessive manner

Oncogenes act in a dominant manner

58
Q

What are caspases?

A
  • Proteolytic enzymes with cytoseines in their active residue, that cleave proteins at aspartate residues
  • Major role in apoptosis (“executioners”)
59
Q

Activation of caspases causes what events to occur?

A

Endonuclease activation
Cell surface alterations
Cytoskeletal reorganization

-All lead to phagocytosis

60
Q

What is the function of Bcl2?

A

Bcl2 prevents the entry into apoptosis. This is over-expressed in some viral infections leading to abnormal growth

61
Q

What diseases are associated with inhibition of apoptosis?

A

Cancer
Autoimmune diseases
Viral infections

62
Q

What diseases are associated with increased apoptosis?

A

AIDS
Neurodegenerative disorders
Ischemic injury

MCBG Exam 3 (5 decks)

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