CELL CYCLE Flashcards

1
Q

WHAT ARE THE TWO CONTROL FACTORS OF THE CELL CYCLE

A
  1. ASSOCIATION OF CYCLINS WITH CDKS

2. MECHANISMS TO STOP THE CELL CYCLE IF THERE ARE PROBLEMS IE CHECKPOINTS

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2
Q

WHAT DECISIONS CAN A CELL TAKE

A

QUIESCENT, PROLIFERATE, DIFFERENTIATE

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3
Q

WHAT HAPPENS IN G1

A

THE CELL GROWS IN PREPARATION FOR DNA REPLICATION AND CERTAIN INTRACELLULAR COMPONENTS UNDERGO REPLICATION

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4
Q

WHAT HAPPENS IN S PHASE

A

THIS IS WHERE DNA IS REPLICATED

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5
Q

WHAT HAPPENS IN G2

A

RAPID CELL GROWTH AND PROTEIN SYNTHESIS

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6
Q

WHY DO CYCLINS DECREASE THROUGHOUT THE CYCLE

A

TO ENSURE THE PROCESS IS UNIDIRECTIONAL

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7
Q

WHY ARE D CYCLINS DIFFERENT

A

D CYCLINS ARE CONTROLLED BY EXTRACELLULAR SIGNALS - INTEGRINS AND ECM ATTACHMENTS

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8
Q

UP UNTIL WHICH POINT IS THE CELL UNDER EC CONTROL

A

R POINT. AFTER R POINT THIS IS A CELL AUTONOMOUS PROCESS. CYCLINS AND CDKS FORM COMPLEXES THAT ACTIVATE THE SUBSEQUENT PHASE AND INHIBIT THE PREVIOUS.

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9
Q

HOW ARE CYCLINS AND CDKS REGULATED

A

CDK INHIBITORS

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10
Q

WHAT INHIBITS CYCLIN D AND ITS CDK4/6 COMPLEXES

A

CKI SUCH AS P16INK4A/P15INK4B/P18INK4C/P19INK4D

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11
Q

WHAT INHIBITS ALL CYCLINS AND THEIR COMPLEXES APART FROM D

A

CKI SUCH AS P57KIP2/P27KIP1/P21CIP1

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12
Q

HOW DO CYCLINS DRIVE THE CELL CYCLE

A

Cyclins drive the events of the cell cycle by partnering with a family of enzymes called the cyclin-dependent kinases (Cdks). A lone Cdk is inactive, but the binding of a cyclin activates it, making it a functional enzyme and allowing it to modify target proteins.

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13
Q

CYCLIN CDK COMPLEXES AT WHICH STAGES

A

G1: CDK4 and CDK6 depend on the association with cyclin Ds (D1,D2 &D3 = D-type cyclins)
After the R point: E-type cyclins associate with CDK2  phosphorylation of substrates required for entry in S phase
S phase: A-type cyclins replace E cyclins in complex with CDK2 - S phase progression. Later in S-phase, A-type cyclins associate with CDK1
G2: B-type cyclins replace A-type ones in the complex with CDK1
M phase: B-type cyclins/CDK1 - mitosis triggering
G0 to G1: mediated by cyclin C/CDK3 complex

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14
Q

WHAT IS THE RESTRICTION POINT FOR

A
  1. IS THE CELL BIG ENOUGH
  2. IS THE ENVIRONMENT FAVOURABLE
  3. IS THERE ANY DNA DAMAGE
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15
Q

WHAT IS G2 CHECKPOINT FOR

A
  1. IS ALL DNA REPLICATED
  2. IS THE CELL BIG ENOUGH
  3. IS THE ENVIRONMENT FAVOURABLE
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16
Q

WHAT IS THE METAPHASE CHECKPOINT FOR

A

ARE THE CHROMOSOMES ALIGNED ON THE SPINDLE

17
Q

HOW DOES THE RESTRICTION CHECKPOINT OCCUR

A
  1. CYCLIN D AND CDK4/6 FORM A COMPLEX IN G1
  2. THIS COMPLEX ALLOWS PHOSPHORYLATION OF PRB (THAT IS BOUND TO E2F)
  3. PHOSPHORYLATION OF PRB INACTIVATES THE PROTIEIN THEREBY FREEING E2F TO BE TRANSCIBED
  4. TRANSCIPTION OF E2F PRODUCES CYCLIN E AND CDK2 ALLOWING PROGRESSION TO S PHASE

E2F REGULATIONS EXPRESSION OF CDK2 , CYCLIN E AND A
IF THERE IS SIGNICANT DNA DAMAGE P53 STIMULATES PRODUCTION OF P21
P21 INHIBITS ALL CDK COMPLEXES WHICH CAUSES ARREST OF THE CELL CYCLE
TUMOUR SUPPRESSOR RETINBOBLASTOMA PROTEIN INHIBITS E2F EXPRESSION
CYCLIN D AND ITS CDK4/6 COMPLEXES PHOSPHORYLATE PRB WHICH LEADS TO ITsINACTIVATION LEADING TO EXPRESSION OF E2F
E2F CAUSES EXPRESSION OF CYCLIN E AND CDK2 THEREBY S PHASE CAN CONTINUE

18
Q

WHAT HAPPENS UPON DETECTION OF DNA DAMAGE

A
  1. ATM/ATR ASSOCIATES WITH SITE OF DAMAGE
  2. THIS ACTIVATES KINASES SUCH AS CHK1//CHK2
  3. THIS CAUSES PHOSPHORYLATION OF P53
  4. P53 CAN CAUSE P21 GENE TO ACTIVATE ENCODING CYCLIN DEPENDENT KINASE INHIBITORS THEREBY ARRESTING THE CELL CYCLE
19
Q

WHAT ARE THE CHOICES OF A DAMAGED CELL AND HOW CAN THIS CHANGE

A

A DAMAGED CELL CAN ARREST UNTIL DAMAGE IS REPAIRED, IF IN G1 IT CAN REVERT TO G0 OR IT CAN TRIGGER APOPTOSIS. THE BALANCE BETWEEN REPAIR AND APOPTOSIS CAN CHANGE OVER TIME.

20
Q

WHAT ACCOMPANIES FORMATION OF MOST TYPES OF CANCER CELLS

A

DEREGULATION OF RESTRICTION POINT DECISION MAKING MACHINERY

21
Q

WHAT IS THE IMPORTANCE OF S PHASE

A
  1. DNA MUST BE REPLICATED ACCURATELY

2. DNA MUST BE COPIED ONCE

22
Q

WHAT IS LICENCING

A

IN G1 INACTIVE HELICASES ARE LOADED ONTO REPLICATION ORIGINS TO FORM A PRE RC WHICH ARE ACTIVATED IN S PHASE BY S PHASE CDKS

23
Q

IS THE CELL CYCLE ALWAYS THE SAME

A

NO, DIFFERENT CELL TYPES IE ESC AND FIBROBLASTS HAVE DIFFERENT CYCLIN PROFILES THAT ARE NOT FULLY UNDERSTOOD.