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Chapter 12: The Cell Cycle Flashcards

1
Q

Stages of cell cycle

A

G1 (first gap), S (synthesis), G2 (second gap), M (mitotic)

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2
Q

Main event during S phase

A

DNA replication

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3
Q

Main event during G2 phase

A

Centrosome duplication

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4
Q

Mitotic spindle consists of

A

Fibers made out of microtubules (some from cytoskeleton)

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5
Q

Microtubules are made up of

A

a- and B- tubulin dimers (proteins)

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6
Q

Centrosome

A
  • Microtubule-organising centre (MTOC)
  • Where the pair of centrioles is located
  • Where assembly of spindle microtubules start
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7
Q

What happens during prophase?

A
  • mitotic spindle begins to form

- centrosomes move away from each other (partly due to lengthening MTs)

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8
Q

By the end of prometaphase, Centrosomes are

A

At opposite poles of the cell

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9
Q

The spindle includes

A

Two centrosomes, spindle MTs, and two asters

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10
Q

Spindle MTs attach to kinetochores during

A

Prometaphase

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11
Q

Metaphase plate

A

An imaginary plate in the middle of the cell on which centromeres are aligned on

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12
Q

What happens during prometaphase? (3)

A
  • Nuclear envelope disintegrates
  • Kinetochore MTs attach to kinetochores
  • Non-KT MTS interact and overlap
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13
Q

What happens during metaphase? (3)

A
  • centrosomes are at opposite poles of the cell
  • Chromosomes are aligned at the metaphase plate
  • MTs of Asters have grown and are attached to the plasma membrane
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14
Q

Aster

A

A radial array of short MTs extending from each centrosome

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15
Q

Separase

A

An enzyme that cleaves cohesins holding sister chromatids together

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16
Q

Two mechanisms for sister chromatid movement:

A

1) Depolymerisation of microtubules at kinetochore ends after passing through motor proteins
2) Depolymerisation at the poles as motor proteins “reel chromosomes in”

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17
Q

Function of nonkinetochore microtubules during anaphase

A

Elongate the cell

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18
Q

In which phases can microtubules lengthen?

A

Prophase and anaphase (non-kinetochore)

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19
Q

What is on the cytoplasmic side of the cleavage furrow?

A

Contractile ring of actin microfilaments associated with myosin

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20
Q

Traditional drawstring model

A

Myosin causes antiparallel actin to slide past each other

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21
Q

Where do vesicles containing cell plate material come from?

A

Golgi apparatus

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22
Q

How do animal and plant cells undergo cytokinesis?

A

Animal: Cleavage furrow
Plant: Cell plate

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23
Q

Describe binary fission.

A

Cell division in prokaryotes, where cell grows to double its size and divides into two

24
Q

How many origins of replication on E.coli?

25
How does one copy of the origin move to the opposite pole of the cell?
Polymerisation of actin-like protein
26
Roles of tubulin in eukaryotic VS prokaryotic cells
Forming microtubules VS cytokinesis
27
How does the tubulin-like protein help split the prokaryotic cell into two?
It pinches the plasma membrane inward
28
Division in Dinoflagellates (nuclear envelope, microtubules, chromosomes)
- nuclear envelope intact - chromosomes attached to n.e. - microtubules pass thru nucleus in cytoplasmic tunnels - division like binary fission
29
Division in diatoms and some yeasts (nuclear envelope, microtubules, chromosomes) ,
- nuclear envelope intact - spindle within the nucleus - chromosomes pulled apart by microtubules
30
Division in most eukaryotes (nuclear envelope, microtubules, chromosomes)
- nuclear envelopes break down - spindle forms outside nucleus - microtubules pull apart chromosomes
31
Division in bacteria
- no nucleus (membrane-bound organelle) - circular DNA - origins of replication - no microtubules
32
Important checkpoints in cell cycle
G1, G2, M
33
Concentration of protein Kinases
Stays constant
34
Concentration of cyclin
Rises during S and G2 phases, falls abruptly during M phase
35
Go-ahead signal at G2 checkpoint
Cyclin-Cdk complex
36
Function of MPF
1) Phosphorylation of various proteins of nuclear lamina 2) chromosome condensation 3) spindle formation
37
Mechanism of switching off MPF
Destruction of cyclin during anaphase
38
Concentration of MDF
Rises and falls during M phase
39
Presence VS absence of go-ahead signal at G1 checkpoint
usually completes G1-M phases VS switches to G0 phase (non-dividing)
40
Go-ahead signal for Anaphase to occur
All sister chromatids are attached to spindle fibres
41
Regulatory molecule during anaphase
Protein complex
42
Outline the reasons for uncontrolled cell division in cancer cells (7)
1) Lack of density-dependent inhibition and anchorage dependence 2) Growth factors in culture medium not needed for growth 3) Faulty cell cycle control 4) Cells stop dividing at random points in the cycle, rather than at normal checkpoints 5) Can divide indefinitely with enough nutrients 6) Has telomerase, which functions to maintain telomere length and prevent cell from undergoing replicative cell senescence/apoptosis 7)Evade apoptosis when mistake has occurred (e.g. during DNA replication)
43
Growth factor
Protein released by cells that stimulate other cells to divide
44
Why do cancer cells not need growth factors in the culture medium?
1) self-produce growth factors 2) Absence of growth factor does not affect signal received by cell cycle control system (i.e. abnormality in signalling pathway)
45
Reason for faulty cell cycle controls
Mutation leading to alteration of protein products
46
Transformation [process; definition]
Process that causes cells to behave like cancer cells (i.e. divide indefinitely)
47
Platelet-derived growth factor (PDGF)
Triggers division of cultured fibroblasts
48
How is signal transduction pathway triggered?
Binding of PDGF molecules to receptors on fibroblasts
49
Cancer cells do not exhibit
Anchorage dependence or density dependent inhibition
50
Benign tumor VS cancerous tumor
Remains at original site VS Spreads to new tissues and organs
50
How do cancer cells undergo Metastasis? (spread of cancer cells to distal organs) (2)
1) Loss of attachment to neighbouring cells and extracellular matrix 2) Signalling molecules that cause blood vessels to grow towards tumor
52
Definition and Effect of Taxol (drug)
Chemotherapeutic drug that stops anaphase by preventing microtubule depolymerisation, thus leading to the cell’s destruction
53
State the two types of Cancer Treatment.
1. Localised tumors: Radiation therapy | 2. Metastatic tumors: chemotherapy—drugs toxic to actively dividing cells circulated in the blood
54
Mechanism of radiation therapy
Damages DNA in cancer cells more so than normal cells, as they do not have the ability to repair damaged DNA
55
Side effect of chemotherapy (+examples)
Affects normal cells that divide often; e.g. nausea → intestinal cells, hair loss → hair follicle cells, reduced immunity → immune system cells
56
Outline the changes observed in cells of malignant tumors, (5)
1) excessive proliferation 2) unusual no. Of chromosomes (May/may not be due to transformation) 3) Altered metabolism 4) Loss of cell-cell adhesion and attachment to extracellular matrix, thus can spread into nearby tissues 5) Secretion of signalling molecules that cause blood vessels to grow towards tumor

SBO (3 decks)

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