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BMS2.20 Cell Division (MILLONIG) > Cell Division > Flashcards

Cell Division Flashcards

1
Q

Deregulated cell growth is the basis of:

A
  • cancer
  • autism
  • cataracts
  • other congenital malformations
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2
Q

The cell cycle control system is:

A
  • Complex network of regulatory proteins that governs DNA replication and segregation of chromosomes through an ordered series of biochemical switches.
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3
Q

The two types/sources of cell cycle control:

A
  • internal
  • external
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4
Q

Role of the internal control system of the cell cycle:

A
  • monitors progression through cell cycle so that each step happens in succession and delays later events until previous ones are completed
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5
Q

Role of the external control system of the cell cycle:

A
  • cells respond to environmental signals in order to stimulate cell division when more cells are needed and to block cell division when no cells are needed.
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6
Q

The cell cycle is:

A
  • the process that a cell duplicates itself and divide to make two daughter cells
    • passing its genetic information to the next generation of cells.
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7
Q

What phase does DNA replication occur?

A

S phase

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8
Q

The two stages of M phase:

A
  • mitosis
    • nuclear division
    • prophase to telophase
  • cytokinesis
    • cytoplasmic division
    • last part of telophase
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9
Q

The four phases of the cell cycle in order:

A
  1. G1
  2. S PHASE
  3. G2
  4. M PHASE
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10
Q

Interphase =

A

G1 + S + G2

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11
Q

Roles of the G1 and G2 phases of the cell cycle:

A
  • Time delay for cell to grow
    • accumulation of mass
  • Time delay allowing for monitoring intra- and extra- conditions.
    • check for mutations, errors, etc.
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12
Q

Restriction point:

A
  • A point that exists at the end of G1 that measures the favorability of the environment.
    • If favorable, cells pass through the restriction point and are committed to DNA replication.
    • Cells are committed to DNA replication once passing restriction point.
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13
Q

What happens if the environmental conditions are unfavorable at the restriction point?

A
  • Cell enters and stays in G0 until conditions become more favorable.
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14
Q

Cell cycle progression is controlled by the sequential activation of (2):

A
  1. cyclin dependent kinases (Cdks)
    • different sets for each part of cell cycle
  2. cyclins
    • necessary for Cdk activity
    • different cyclins for each part of cell cycle
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15
Q

How do Cdks regulate the cell cycle?

A
  • activated by different cyclins, then:
  • phosphorylate different proteins at different times in the cell cycle which then in turns initiates or regulates key events in the cell cycle.
    • i.e. replication, mitosis, etc.
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16
Q

What happens to cyclins once they activate a Cdk, and the event following Cdk phosphorylation is complete?

A

cyclins are degraded via proteolysis

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17
Q

The four classes of CDKs:

A
  • G1 Cdk
  • G1/S Cdk
  • S Cdk
  • M Cdk

EACH Cdk HAS ITS OWN UNIQUE CYCLIN REQUIRED FOR Cdk ACTIVATION

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18
Q

G1 Cdk function:

A

promotes passage through the restriction point

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19
Q

G1/S Cdk function:

A

commits cells to replication

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20
Q

S Cdk function:

A
  • control the initiation of DNA replication once per cell cycle at replication origins.
21
Q

M Cdk function:

A

promotes mitosis

22
Q

What are the molecular switches of the cell cycle?

A

Cdk-cyclin complexes

23
Q

Origin Recognition Complex (ORC) structure and function:

A
  • large, multi-protein complex that binds origins of replication.
  • acts as landing pad for other regulatory proteins to initiate replication at different positions throughout the genome so that the entire genome is duplicated.
24
Q

Cdc6:

A
  • protein usually present at low levels, but upregulated during G1.
  • binds to ORCs, causing the recruitment of the Mcm proteins (helicases)
25
Q

Mcm proteins/complex:

A
  • helicases recruited by Cdc6 binding to the ORC in G1.
  • forms the pre-RC
26
Q

Pre-replicative complex (pre-RC) is composed of:

A

ORC, Cdc6, and Mcm complex

27
Q

Following formation of the pre-RC during G1, S-Cdk triggers replication by (4):

A
  1. Binding to S cyclin.
  2. Assembling the DNA polymerase and other replication machinery at the origins.
  3. Activating the Mcm proteins to slide along the DNA and act as helicases.
  4. Phosphorylating the DNA replication machinery.
28
Q

S-cyclin transcription is activated when?

A

in late G1

29
Q

How is re-replication prevented during G1?

A
  • S-Cdk phosphorylates Cdc6.
    • causes Cdc6 to dissociate from ORC after origin has fired for replication.
    • results in the disassembly of pre-RC, which prevents replication from occurring at same origin.
  • S-Cdk phosphorylates Mcm/helicase proteins.
    • causes their export from the nucleus.
30
Q

How is re-replication prevented during G2 and M?

A
  • S-Cdk activity remains high during G2 and mitosis.
    • phosphorylates Cdc6 protein
  • M-Cdk phosphorylates Cdc6 and Mcm proteins.
31
Q

How does the cell cycle control system reset itself to allow replication in the next cell cycle?

A
  • At end of mitosis all Cdk activity is reduced to zero.
    • results in the dephosphorylated Cdc6 and Mcm proteins allowing for pre-RC assembly to occur again.
32
Q

Steps in triggerring and completion of S-Phase:

A
  1. ORC binds to origin of replication.
  2. Unphosphorylated Cdc6 binds to ORC.
  3. Unphosphorylated MCM binds to ORC (Pre-RC).
  4. S-Cdk upregulated. End of G1.
  5. S-Cdk phosphorylates replication machinery.
  6. Replication occurs.
  7. S-Cdk and M-Cdk phosphorylate Cdc6 and Mcm proteins to prevent re-replication.
33
Q

Are S-Cdk and M-Cdk expressed during the beginning of G1?

A
  • No.
    • allows for formation of the pre-RC complex.
34
Q

The regulation of M-Cdk is controlled by what 3 proteins?

A
  • M cyclin.
    • M cyclin which gradually increases during G2 and M phases due to transcription of the gene.
  • Cdk activating kinase (CAK).
  • Cdk inhibitory kinase (Wee1).
35
Q

Steps in M-Cdk activation:

A
  1. M-cyclin binds to M-Cdk (inactive).
  2. Inactive M-Cdk phosphorylated by both CAK and Wee1 (inactive).
  3. Cdc25 phosphatase removes Wee1 phosphorylation from inactive M-Cdk (active).
36
Q

M-Cdk phosphorylates proteins that are responsible for:

A
  • assembly of the spindle for chromosome segregation
  • chromosome condensation
  • breakdown of the nuclear envelope
37
Q

What feedback loops cause increased M-Cdk activity?

A
  • Active M-Cdk:
    1. inhibits Wee1, preventing the inhibition of M-Cdk through Wee1.
    2. phosphorylates Cdc25 phosphatase, activating more of it, so that more of the inhibitory phosphate is removed.

INHIBITS THE INHIBITOR

ACTIVATES THE ACTIVATOR

38
Q

How is M-Cdk inactivated?

(thus, ensuring exit from mitosis)

A
  • Active M-Cdk itself activates an ubiquitin ligase called Anaphase Promoting Complex (APC).
  • Active M-Cdk is then degraded by the proteasome.
39
Q

G1 is a period of no Cdk activity.

What three mechanisms ensure there is no Cdk activity?

A
  1. Ubiquitin mediated degradation of Cdks
  2. Cyclin Kinase Inhibitor (CKI) accumulation
  3. Decreased cyclin transcription
    • Rb and E2F regulate this.
40
Q

Cyclin Kinase Inhibitors (CKIs) function:

A
  • bind to active cyclin-Cdk complexes and inhibit their kinase activity.
  • CKI production is increased during G1.
41
Q

How does the Retinoblastoma (Rb) protein decrease Cdk activity?

A
  • Rb inhibits E2F transcription factor.
    • E2F is required for the expression of G1/S and S cyclins.
    • Rb inhibits E2F during G1 so this causes no G1/S and S cyclin expression.
42
Q

E2F:

A
  • a transcription factor required for the expression of G1/S and S cyclins.
  • Rb inhibits E2F during G1 so this causes no G1/S and S cyclin expression.
43
Q

When cells receive an extra-cellular signal to divide, what occurs to Rb and E2F?

A
  • G1-Cdk accumulates, phosphorylates Rb, reduces the affinity of Rb to E2F which results in the expression of G1/S and S cyclins.
44
Q

E2F regulates its own expression by:

A
  • E2F binds to its own promoter, increasing its expression.
  • E2F expression leads to increase of active G1/S-Cdk and S-Cdk, which:
    • phosphorylates Rb leading to greater inactivation of Rb.
    • enhances phosphorylation of ubiquitin ligases and CKIs leading to their destruction in the proteosome and as a consequence activating more G1/S-Cdk, S-Cdk, and E2F.
45
Q

When are the two DNA checkpoints?

A
  • one in late G1
  • one in late G2
46
Q

G2 DNA Checkpoint:

A
  • DNA damaged, cell wants to block mitosis.
  • Damaged DNA sends a signal that blocks Cdc25 activity.
    • Cdc25 is the phosphatase that removes the inhibitory phosphates put on by Wee1.
    • M-Cdk remains phosphorylated and remains inactive - mitosis does not occur.
47
Q

G1 DNA Checkpoint:

A
  • DNA damaged, cell wants to block S-phase.
  • prevents progression into S phase by inhibiting the activation of G1/S-Cdk and S-Cdk complexes.
    • controlled in part by p53.
48
Q

p53:

A
  • involved in G1 DNA damage checkpoint
  • p53 stimulates the expression of several genes including a CKI protein (p21).
    • p21 binds to G1/S-Cdk and S-Cdk, inactivating them and preventing entry past the restriction point and into S phase.
49
Q

p53 stimulates expression of a CKI (p21), which does what?

A
  • binds to G1/S-Cdk and S-Cdk, inactivating them and preventing entry past the restriction point and into S phase.
  • G1 checkpoint.

BMS2.20 Cell Division (MILLONIG) (1 decks)

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