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CORE II Block 3 > Cell cycle > Flashcards

Cell cycle Flashcards

(40 cards)

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1
Q

What are the phases of interphase?

A

G1, S, G2

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2
Q

What are the phases M phase?

A

mitosis and cytokinesis

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3
Q

Describe several methods to study the cell cycle (including model organisms)

A

model organisms:

  • zebrafish (BrdU and antibody)
  • rat fibroblasts (are round when in mitosis)
  • budding yeast (bud off when mitosing)
  • fission yeast (length is indicative of cell cycle stage)
  • flow cytommetry can measure the content of cells to determine the stage of the cell cycle
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4
Q

How do we know the cell cycle control proteins are highly conserved?

A

you can place proteins from one vertebrate into another and oftentimes the cell cycle functions as normal.

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5
Q

What is the restriction point?

A

It is the point in the cell cycle where DNA replication begins and the cell can not go back.

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6
Q

What is the purpose of the cell cycle checkpoints?

A
  • surveillance systems
  • quality control mechanisms of the genome
  • required for accurate transmission of genetic information
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7
Q

What is the engine of the cell cycle?

A

cyclin-dependent kinases

  • conserved throughout evolution
  • phosphorylate serine or threonine residues of target proteins at K/R S/T X K/R consensus sequence
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8
Q

List the major cyclins and Cdks of the vertebrate cell cycle.

A
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9
Q

Describe the four regulatory mechanisms of Cdks.

A
  1. transcriptional regulation - to control amount of cyclins
  2. phosphorylation/dephosphorlyation of Cdks
  3. Cdk kinase inhibitors - in the control of G1/S- and S-Cdk
  4. ubiquitin-dependent proteolysis -to control amounts of cyclins (in addition to transcriptional control)
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10
Q

Provide an example of the phosphorylation/dephosphorylation of Cdks to regulate their activity.

A

Cdk is first activated by phosphorylation at its active site, regardless of the presence of cycln

M-cdk:

it can be phosphorylated at a second site by Wee1 kinase, inhibiting it

this phosphate can be removed by cdc25 phosphatase, reinstating the activity of cdk

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11
Q

Provide an example of a Cdk inhibitor that controls activity of Cdk.

A

In G1/S- and S-Cdks, p27 may bind the G1/S-cdk and G1/S cyclin complex, restricting access to the active site.

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12
Q

Describe ubiquitin-depedent proteolysis to control Cdk activity by APC/C.

A

In the case of M-Cdk:

Cyclins can be degraded by ubiquitination by APC/C when it is in its active state. APC/C is normally inactivated by Cdc20

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13
Q

Describe ubiquitin-depedent proteolysis to control Cdk activity by SCF.

A

promotes S-phase entry:

  • an active SCF complex contains an F box protein with catalytic activity
  • F box ubiquitinates CKI protein when it is active and phosphorylated, allowing for the G1-S transition.
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14
Q

How do S-Cdks license the cell to only replicate DNA once per cycle?

A

Cdc6 and Cdt1 are licensing factors involved in forming the pre-replicative complex at the ORC. At this point, S-Cdk is active and causes origin firing. It also phosphorylates cdc6 and cdt1, marking them for degradation so that another replicative complex cannot be formed.

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15
Q

When and how is sister chromatid cohesion established?

A

Sister chromatid cohesion is established in S phase, after DNA has been replicated.

  • In M1-S, cohesin is loaded around DNA molecule.
  • In S, cohesion is established as cohesin proteins line up at replication forks. The two daughter molecules pass through rings of cohesin.
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16
Q

List the stages of mitosis.

A
  1. prophase
  2. prometaphase
  3. metaphase
  4. anaphase
  5. telophase
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17
Q

Describe the G2-M transition and how M-Cdk drives entry into mitosis.

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A

Once Cdk1 is bound by cyclin and activated by Cdk-activating kinase, it is often inhibited by Wee1 kinase. Cdc25 will come along and remove this inhibitory phosphate, reactivating Cdk1. Activation of Cdk1 acts as a positive feedback loop, as it inhibits wee1 kinase and activates cdc25 phosphatase, leading to the accumulation of Cdk1 after the initial activation of one molecule.

18
Q

Describe in detail the condensation of DNA. When does this take place?

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A

DNA is condensed into chromosomes during prophase of the M phase.

  • condensin catalyzes the restructuring and compaction of chromosomal DNA.
  • condensin is similar in structure to cohesin. It contains the Smc proteins organized into a ring structure, with 3 non-SMC proteins.
  • by metaphase, we can see siste chromatid resolution
19
Q

Describe nuclear envelope breakdown. During what phase of mitosis does this occur?

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A

Nuclear envelope breakdown occurs during prophase, prometaphase, and metaphase. It is facilitated by M-Cdk

  • M-cdk phosphorylates some proteins in nuclear pore complexes, the nuclear lamins, and inner nuclear envelope proteins
  • this causes disassembly of nuclear-pore complexes and the breakdown of nuclear membranes into small vesicles
  • this leads to the release of motor proteins and microtubule regulators from the nucleus to the cytoplasm for mitotic spindle formation
20
Q

Describe mitotic spindle formation. When during mitosis does this take place?

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A

Mitotic spindle formation takes place during prophase, prometaphase, and metaphase of mitosis.

  • astral microtubules contact the cell cortex
  • kinetochore microtubules attach to sister chromatids via their kinetochores.
  • interpolar microtubules overlap with the plus ends of microtubules from the opposite pole to form an antiparallel array at the midzone
21
Q

Where are the mitotic spindle poles located? How do these structures duplicate?

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A

They are assembled at opposing centrosomes. These are made up of two centrioles each, surrounded by a pericentriolar matrix consisting of:

  • microtubule-dependent motor protiens
  • gamma tubulin (responsible for nucleating microtubules)

Centrosome duplication is promoted by G1/S-Cdk. The two centriole pairs remain close to one another until ready for mitotic spindle formation. Centrosomes replicate in a semiconservative manner, just like DNA.

22
Q

How is the assembly and function of the bipolar mitotic spindle governed?

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A

It is governed by Microtubule-dependent motor protiens:

  • kinesins move towards plus ends
  • dyneins move towards minus ends (help position mitotic spindle in cell via astral microtubules)
  • they push and pull microtubules to separate the spindle poles
23
Q

How are motor proteins which govern mitotic spindle formation activated?

Study These Flashcards
A

Kinesin and dynein are activated by phosphorylation by M-Cdk,polo-like kinase, and aurora kinases A and B.

24
Q

How do kinetochores attach sister chromatids to the mitotic spindle?

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A
  • spindle microtubules attach to the outer region of large kinetochore complex
  • kinetochore complex forms at centromere region of chromosome
  • plus ends of microtubules are embedded in the fibrous part of the kinetochore that contains Ndc80.
  • Ndc80 attaches to the sides of microtubules, so they can continue to polymerize and depolymerize.
25
Describe how the bi-orientation of spindle attachment to kinetochores is achieved.
Bi-orientation is achieved by tension to position chromosomes at the metaphase plate. - tension is created by microtubules attaching to both sides of kinetochores and by sister chromatid cohesion. - Improper spindle attachment causes low tension and instability - proper attachment leads to high tension and stability, allowing chromosomes to be positioned at the metaphase plate. This is achieved by trial and error.
26
How is tension created between chromosomes and the mitotic spindle?
- low tension is a result of phosphorylation of Ndc80 by aurora B (tethered to the inner kinetochore) kinase, decreasing the affinity between Ndc80 and plus ends of microtubules - high tension is achieved when there is more distance between Ndc80 and aurora B, so Ndc80 cannot be phosphorylated. This allows for a high affinity between microtubules and Ndc80, causing a stable bi-oriented spindle.
27
How is sister chromatid separation and the completion of mitosis triggered?
APC/C promotes this: - causes ubiquitination of both securin and cyclin B (no more M-Cdk) - loss of securin allows separase to break cohesin rings holding sister chromatids together.
28
How is the cell cycle affected when steps go wrong with the mitotic spindle?
The spindle assembly checkpoint regulates APC/C: - ensures correct separation of chromosomes at mitosis and meiosis - blocks the metaphase-anaphase transition until all chromosomes are properly attached to the mitotic or meiotic spindle - If not properly attached, checkpoint protein Mad2 is recruited to unattached kinetochores and bind APC/C, inhibiting it so that securin remains active - if proper attachment is achieved, checkpoint protein is released from APC/C and securin is ubiquitinated, causing separase to become active
29
Describe chromosome segregation in anaphase A and B.
Anaphase A: - initial poleward movement of chromosomes by shortening of kinetochore microtubules. - chromosome movement is dependent on force generated by microtubule depolymerization at kinetochore as well as microtubule flux (the poleward movement due to minus-end polymerization) Anaphase B: - the two spindle poles move apart fully - spindle pole separation depends on a motor-protein driven mechanism - anaphase completion also depends on dephosphoryulation of M-Cdk substrates.
30
Describe telophase.
- chromosomes arrive at the poles - mitotic spindle begins to disassemble because of the loss of M-Cdk activity - the nuclear envelope begins to assemble and daughter nuclei form - cytoplasmic division begins with contraction of the contractile ring - chromosomes decondense
31
What generates the force needed for cytokinesis?
the force is generated by actin and myosin II in the contractile ring: - preparation begins in interphase as actin and myosin II form a cortical network undelying the plasma membrane - at onset of M phase, actin and myosin II disassemble and start to reorganize - at anaphase, actin and myosin II accumulate to assemble the contractile ring - curing cytokinesis, the contractile ring contracts to generate the force the divides the cytoplasm in two, creasting the cleavage furrow to divide the cell. Chromosomes are then decondensed and surrounded by a new nuclear envelope.
32
How is the assembly and contraction of the contractile ring triggered?
Rho GTPase is activated at cleavage sites and triggers assembly/contraction of contractile rings: - RhoA is activated when bound to GTP (after exchanging GDP with the GEF) - It can also be inactivated by a RhoGAP which hydrolyzes its GTP to GDP. - RhoA promotes actin filament formation via formin - promotes myosin II assembly via Rock (Rho-activated kinase) which inhibits myosin phosphatase and stimulates phosphorylation of myosin regulatory light chain, activating myosin II and allowing for ring contraction
33
How are organ and body size determined?
- cell division - cell growth - cell survival
34
How are cell division, cell growth, and cell survival regulated?
- They are controlled by intracellular programs and by extracellular signals which control these programs. - extracellular signals are mitogens (cell division), growth factors (cause cell growth), and survival factors (suppress programmed cell death) - extracellular signals that suppress cell growth, division, and survival are stress such as DNA damage (suppresses cell cycle/division) and signals that activate apoptosis (such as Fas on a CD8 cell)
35
How do mitogens stimulate cell division?
Mitogens stimulate cell division by activation of G1- and G1/S-CDKs - early on in the cell cycle, mitogens bind mitogen receptors, such as RTKs, activating Ras GTPase - Ras activates MAP kinase cascade, leading to expression of Myc. - Myc activates G1-Cdk (cyclin D and Cdk 4/6) which phosphorylates Rb, inactivating it - inactivation of Rb releases E2F transcription factor, allowing it to transcribe genes involved in S phase such as G1/S- and S-cyclins
36
What happens to the cell cycle in the event of DNA damage during G1/S checkpoint?
DNA damage elicits negative signals to arrest the cell cycle: - damage activates ATM/ATR kinases, causing Chk1 and Chk2 kinase activation - these checkpoint kinases phosphorylate p53 so it is no longer bound and ubiquitinated by Mdm2 - p53 binds regulatory region of p21 gene, causing its expression. - p21 acts as a CKI to bind and inhibit G1/S and S-Cdks.
37
What happens to the cell cycle in the event of DNA damage during the G2/M checkpoint?
- checkpoint kinases are activated much as it is when there is DNA damage during G1/S. - Chk1 and chk2 activate wee1 kinase and inhibit cdc25 phosphatase, leading to the inactivation of M-cdk
38
List three major roles of p53.
1. txn of p21 2. initiates apoptosis 3. initiates senescence
39
Which checkpoints are stalled by DNA damage?
1. G1/S cdk 2. S cdk 3. M cdk
40
Describe the pathway of cell growth which accompanies cell division.
- growth factor binds and activates RTK, leading to phosphorylation and activation if PI3K. - PI3K activates mTOR which activates S6K (S6 kinase) - S6K acts on S6 ribosomal protein, promoting the activity of ribosomes to increase protein synthesis and cell growth (must replicate all the proteins before division!) - mTOR also activates eIF4E, initiating more translation - mTOR is also activated by nutrients, because mTOR is a nutrient-sensing kinase

CORE II Block 3 (7 decks)

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