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BIOL311 > Cell Division > Flashcards

Cell Division Flashcards

1
Q

Caner

A

Unregulated Cell division

***cancer = relates to cell division

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2
Q

Cells + nucleus

A

Some cells do not have a nucleus

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3
Q

Cells without a nuclues

A
  1. RBCs
  2. Human Skin
  3. Lens of the eye
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4
Q

RBCs

A

Simple cell that can replicate – bag of hemoglobin

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5
Q

Human RBCs vs. other animals RBCs

A

Humans = RBCs do not have a nucleus

Aviation + Amphibians (birds + frogs) = RBCs do have a nucleus

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6
Q

Amatopoisis

A

Shed nucleus

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7
Q

Human Skin Layers

A

Bottom layer = has nuclei

Strayum Corneum = No nucleus –> has cells but as the cells move up to the top they lose their nuclei –> allows the cells to compress = makes barrier properties

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8
Q

Why does the Starum Corneus lose nuclei

A

So that as the cells move up they can compress = gives it barrier properties

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9
Q

Lens of the eye Shape

A
  • In lenticular shape
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10
Q

Layers of lens

A
  1. Has epithelial Layer
  2. Has germal layer
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11
Q

Lens of the eye division

A

Cells divide in the lens at the equator in the GERMAL LAYER –> as they divide = they differentiate into lens fiber cell with crystals

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12
Q

Lens over lifetime

A

Lens throughout your whole life = keeps growing –> reason old people get glaucoma

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13
Q

Lens fiber

A

No nucleus (Anuclease)

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14
Q

Enucleated

A

Verb!!! – like in SCNT when you enucleate (remove the nucleus)

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15
Q

Why shouldn’t lens have nuclei

A

Relates to phase microscopy –> because you can see differnt patrts of the cell in a phase microscope because of diffreent refractive indicies –> This would happen in the lens if it had a nucelus
- Having a nucelus would ruin your ability to see because it would interfere with refractive indicies

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16
Q

Parts of the Nucleus

A
  1. Nuclear envelope
  2. Nuclear Pores
  3. Histones
  4. Non-Histones
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17
Q

Nuclear envelope

A

Double membrane system around the nucleus
- Comes from the ER
***NE = connected to the ER because the ER generates the Nuclear Envelope

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18
Q

Nuclear Pores

A

VERY COMPLEX
***Sites where mRNA + Proteins leave

Use - passivley diffuses proteins less than 62,500 da

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19
Q

Diffusion of nuclear proteins

A

Most proteins in nucleus = can diffuse passively through nuclear pores BECAUSE most of the proteins in the nucleus are Histones

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20
Q

Histones

A

Small 20,000 da proteins in the nucleus –> they can diffuse passively through nuclear pores
***Most proteins in nucleus = histones

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21
Q

Use of Histones

A

Involved in Epigenetics – can be methylated + Phosphorylated

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22
Q

Non-Histones

A

Includes Transcription factors + Other proteins
- Have many different molecular weights

Example – Lamins (Type of intermediate Filament)

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23
Q

Example Active transport

A

Nucleoplasm (Nuclear protein) – exceed the passive diffusion weight
- Big protein = 165,000 da = can’t diffuse
- It is a Pentomer –> 5 SU each 33,000 da
- First molcular chaparone discovered

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24
Q

Discovery of Nucleoplasm

A

Found originally in African frog toad – found in Xenous Leavits

10% of the protein in the X. Laeveis egg

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25
Q

Where do xenobots come from

A

X.levits

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26
Q

Function of Nucleoplasm

A

Chaperone + nucleosome assumably + Genome stability + Transcriptional regulation

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27
Q

Purpose of Nucleosome

A

Helps histones arrange

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28
Q

Synthesis of Nucleosome

A

Question – is it synthesized in the cytoplasm and then shipped through a pore?

Experiment – track synthesis:
***Use ultrastructural radiograhy
- Use gold labeled anti-nucleoplasm tag – use Ultrasturctural radiography

  - Idea = that it uses an ATP dependint synetshis to be trasnported through the pore SO you want to remove ATP BUT you can't remove all ATP or the cell will die -- SOLUTION = cool the cell to 4 degrees celcius

Result: Nucelosome gets transported through the nucleo pore

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29
Q

Lamins

A

Overall – type of intermediate filament

Found – in the inner envelope of nucleus

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30
Q

Types of Lamins

A
  1. Lamin A
  2. Lamin B
  3. Lamin C
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31
Q

Function of Lamins

A

Functionally important because they have many functions

  1. Provide structure for keroskeloton – important for circularization of the nucleus + localizing it in the center of the cell
  2. Connects chromatin to nucelar envelop – at the nuclear pore
  3. Phosphorylation of Lamin B triggers nuclear dissolution (MOST IMPORTANT FUNCTION)
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32
Q

Nuclear Dissolution

A

Nuclear envelope disappears

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33
Q

Inducing nuclear dissolution experiment

A

Experiment = demonstrates nuclear dissolution occurs during mitosis

Exp:
Fuse a mitotic cell with a cell in G1

Results:
1. Get nucleus disappears = have nuclear dissolution
2. G1 chromatin condenses –> means that something in the mitotic cell that can cause premature formation of chromosomes

***Some entity (MPF) = causes nuclear dissolution via Lamin Phosphorylation

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34
Q

Lamin + Nucleus

A

Have lamin inside nucleus –> when nucleus goes through mitosis = have nuclear dissolution + lamin B is phosphorylated (triggers dissolution)

Late mitosis – lamin B is dephosphorylated BUT doesnt mean that Lamin B comes back to make new nuclues –> the new nucleus comes from the ER

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35
Q

Defect in Lamin A

A

Associated with progeria

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36
Q

Progeria

A

Precoccious aging disease – age faster

Issue = not elliptical nucelus –> mishappen nuclei – not spherical

Normal – the Fornesyl comes off after the lamin is insertes –> Normal = have Lamina around the rim

Affected – The fornesyl stays on – make the Lamin BUT the Fornesyl foes not come off in the end = cause smishapen nucleus

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37
Q

Lamin Assmebley

A

Known process – know that formesyl inserts lamin into memebrane
***Faciliates lamnin into nuclear envelope

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38
Q

Lonafarnib

A

Farneyltrasnferace inhibitor used to treat Progeria
***Farneyltrasnferace inhibitor = researched a lot in cancer because Farnesyl links ocoproteins = get cancer but the inhibitors didn’t help

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39
Q

Cell Cycle (overall)

A

G0 –> G1 –> Restiction/START point –> S (DNA synthesis) –> G2 –> M phase (mitosis) –> daughter cells

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40
Q

What is cell cycle related to

A

Relates to embryogenesis + Stem cells

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41
Q

Fidelity of cell division

A

Remarkable –> to not make mistake

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42
Q

Cell division Occurance

A

Cell divison = occurs all of the time –> theoretically you should get bigger – Need a balance between cell division and cell death

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43
Q

Hematopoeis

A

Type of cel division – RBC division

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44
Q

G0

A

First part of cell cycle
***Technically NOT part of G1
- Quecet period –> part of the cell cycle chrachteristic of differenated cell

***Cells in G0 have no interest in dividing unless they are triggered to do so

45
Q

What does G stand for?

A

Gap – gap between mitosis

46
Q

G1

A
47
Q

G1 length

A

For a cell that has a cell cycle of 24 hours –> 9 hours

G1 = 9/24 hours

48
Q

Cancer cell cycle

A

Cancer cells can’t go through the cell division any faster

Example – some cancer cell cycle = 38 hours

49
Q

Aurthur Pardee

A

Looked at G1 cycle – looked at the cell cycle in general BUT he mostly looked at G1

Asked – what does it take to get through G1 – what do you need to get from G1 –> DNA replication

Results: Found that you need Growth factors

50
Q

Cells authur used

A

Used 3T3 cells – easy to convert from normal to cancer cells
**He introduced 3T3 cells – made them famous
**Commonly used for cell cylce and oncogene studes because they are easy to convert from normal to cancer cells
***They are isolated from mouse embryo tissue

51
Q

What did authur show?

A

Showed that you need Growth factors to get from G1 –> S phase

Need PDGF –> EGF –> Insulin – need the growth factors in THAT order

PDGF –> EGF –> Insulin (ALL before S)

52
Q

Genes in G1

A

Can identrify early and late response genes – All activated by Growth factors

To Study – look at mRNA over time

Results:
1. Get early response genes (see increase in mRNA early)
2. See late response genes (increase in mRNA later)

53
Q

Early + late response genes

A

If you prevent the degradation of early response genes = then you don’t get the late response genes = SHOWS that they are connected

***Don’t get late response without the early

54
Q

Studying Cell cycle

A
  1. Most of the work done = done by fusing cells
  2. Need to synchronize the cells so that they are all going through the cell cycle at the same time – to study you need cell synchrony (doesn’t occur naturally – need to induce it)
55
Q

Inducing Cell synchrony

A

It won’t occur natural – you need to induce it
***Most wats are based on G1

  1. Amino Acid deprivation – stall cells in G1 –> because no AA = the cells can’t make proteins = stalls
    • Can add back later
  2. Serum deprivation – stalls in GA (Prefered way)
    - remove growth factors
  3. Protein synthesis inhibtors – stalls in G1 + can stall in G2 (since it can stall in both = this is not prefered method)
  4. DNA synthesis inhibition – stalls in S
  5. Nucleosome inhibitor – stalls in M because spindle us inhibited
56
Q

Cell synchrony experiment

A

Take synchronized cells and watch them divide

Result: Get a graph with a very strange profile –> need to figure out what happened
- Found that the only way to get that data was if the cell cycle was 24 hours +/- 6 hours – means that the cycle is varaible

57
Q

What part of the cell cycle is variable

A

G1 phase – most variable in time

Variability = explains why the cells fall out of synchrony over time

58
Q

Two points in the G1 cycle

A
  1. G1 checkpoint
  2. Resiction point
59
Q

G1 checkpoint

A

Checking fidelity of process –> anylzye the fidelity (correctness) of G1 process
***Look at DNA

60
Q

G1 restiction point

A

G1/S boarder – Go or no go point
***At this point – goes to S phase

IF it doesn’t go to S = it goes backwards in G1 = spends more time there

***aka “pardee point”

61
Q

Where is restiion point found

A

Found in mammal cells + non-mammal cells BUT not in yeast cells

***Start in yeast

62
Q

Do cancer cells differ from normal cells in their repsective cell cycle conpartment time?

A

Answer – they are not different

Experiment – look at different compartment times (look at each separately)

Take G1 synchronized cells – take synchrionized cells and watch

  1. In G1 –> Add H3-thimadine –> Look at how much time it is before you see labeled cells – because the labeled cells = tell you they are in S phase
    • Once see labeled cells = know they are done in G1 – now in s (Because they are doing DNA replication)
  2. In S –> look at randomly dividing cells – all go through the cell cycle at different times
    • At H3-thiamdine –> look at the number of labeled cells – if 3/10 are labeled = then do 3/10 X 24 hours = gives you the S phase time
  3. G2 Time –> use randomly dividing cells again
    • Use H3 thiamdine to pick only cells in S phase –> once they are in M = you will see lableed chromsomes
    • can see m cells with radioactive probe = tells you length of G2
      - can use the same system to find length of m Phase

Result: Normal cells + cancer cells = have the same compartment times

63
Q

Adding H3-Thimadine

A

Add to cells to probe cells that are going through DNA replication (cells starting to divide)

64
Q

What controls cell cycle transit

A

Cyclins + associated Cyclin dependent kinases

65
Q

Rhudamin + hunt

A

Did classic experiment about cell cycle movement

Exp:
Took naturally occuring synchronized cells – used sea urchin embryos (used ionmycin or sperm – added at once to the eggs)

THEN they ran SDS gel to see proteins

Results: Discovered Cyclins

66
Q

Types of cyclins

A

There are many BUT only two are important:
1. Cyclin B
2. Cyclin A

67
Q

Mitotic Cyclins

A

Cyclin A and Cyclin B – govern whether the cell goes through mitosis

68
Q

What is associated with cyclin

A

Cyclins have partner cyclin dependent Kinases
***Cyclins won’t do anything unless has partner CDK

NEither alone can do anything –> they are a pair
***They can be influenced by many things – many things inhibit their function

69
Q

CDKs

A

CDKs = increase and decrease over the cell cycle

70
Q

Amounts of Cyclinc over cell cycle

A

Cyclin e – G1 –> S
Cyclin A –> G1 –> S –> G2 (decrease at m)
Cyclin B – M phase
Cyclin D –> G1

71
Q

Mitosis

A
72
Q

What is required for G1 passage

A

Cyclin D
***Cyclin D = associated with G1

73
Q

Cyclin D experiment

A

Questioon – Us Cyclin D required for G1 cell cycle transit
T
ake G0 cell –> Add Growth factors –> Add BrdU –> Look at BrDU incorporation after time

Control cell – leave alone
- Result: have BrdU positive cells – means they are in S phase

Experimental cell – add anti-cyclin D antibody – blocking cyclin D
- Result: BrdU negative cells

***BrdU = like H3-Thiamine BUT safer

If add AB early in G1 = the control go to S BUT the experimental do not

If add AB late in G1 = the conrtol go to S and the experimental go to S (if add the antobody late in G1 = teh cells still go to S phase)

74
Q

Use of BrdU

A

BrdU = like H3-thiamine BUT is safer – floursecnt alternative to H3-Thimadine

75
Q

S phase

A

DNA synthesis

76
Q

How do we study S phase

A

We can use electron microscope to tell us about S phase

Exp – Take cells in S phase –> Open cells + open the nucleus

Result: See replicons/replication bubbles – bubbles tell you there may be multiple points of replication + DNA synthesis may be directional

77
Q

Two ways to study S phase

A
  1. Elecrton microscope
  2. Use Fiber autoradiogrphy
78
Q

Autoradiography in S phase

A

Use fiber Autoradiography – Use autoradiography with chromosome inside –> Shows that electron microscope were right

79
Q

Replication origins

A

Know there are many points where replication generates + H3 thiamine incorporates

Have Point ORC –> ORC makes replication bubble

80
Q

What controls S phase

A

Cyclin A-CDK –> move cell cycle to mitosis

81
Q

Cyclin B

A

Main mitotic cyclin

82
Q

G2 phase

A

Some protein synthesis is required
***We know very little about G2 because non one cares about G2 = no one studies G2

83
Q

What Happens in G2

A
  1. Cell verifies that al of the DNA has been correctly duplicated and all DNA errors have been corrected
  2. Chromosome condensation is initiated
  3. Early organization of the cell cytoskeleton
  4. Mitotic cyclin dependent kinases initiate activity
84
Q

Mitosis (Overall)

A

Prophase – Spindle poles
Metaphase – sister chromatids
Anaphase
Telophase + Cytokinesis

85
Q

M phase

A

***get new nuclear envelope

86
Q

Shortest Phase in Cell cycle

A

M phase – know by looking at cell kinetic studies

87
Q

Lamins in M phase

A

Lamin B = gets phosphorylated by MPF

88
Q

What triggers movement through M Phase

A

MPFs

E.Leavis – Maturation phase factor
Mammalian cells (Cell fusion) – Mitosis Phase factor

89
Q

Discovering MPF

A

2 groups using 2 model organisms:
1. Using X.levais –> perfect organism to study because cycles go through sequence
- take cytoplasm out of cell –> put in new cell –> idnduces mitosis iommediatley = have factors to promote maturing in egg
Found MPF – Matruartion Phase factor

  1. Used cell fusion experiment –> tells you what tells cell to go through mitosis
    Overall – took a test tube + added cytoplasm from mitotic cell + nucleus + ATP –> Nucleus will duplicate
    Used mammalian cells –> Did cell fusion –> found MPF
    MPF – Mitosis Phase factor
90
Q

Use of MPF

A

MPF = phosphorylates Lamin B = causes nuclear dissolution

91
Q

When is MPF highest

A

MPF = highest at Metaphase

92
Q

MPF cycle

A

Metaphase = high MPF –> In anaohase the Cyclin B is uqiquinated = decrease cyclin B BUT still high CDK–> make more cycle B over the course of the cycke = have more at mitosis again

Low MPF at telophase

93
Q

What is MPF

A

MPF = Cyclin B + CDK

94
Q

MPF function

A

Phosphorylate Lamin B = have dissociation of nuclear envelope = reason why MPF is high during metaphase

95
Q

Cyclins in Cell cycle

A

Cyclin A = S phase + G1
Cyclin B = M phase
Cyclin D = specific to different cell cycle points

96
Q

Ruth Sager

A

Discovered Cell cycle check points

***First to suggest that we have tumor supressor genes –> first to suggest that we have genes in system to prevent cancer

97
Q

P53 (chart)

A
98
Q

Cell cycle Checkpoint

A

Sites of control – we have many cell checkpoints
***Each cell cyle compartment = has checkpoint – check fidelity

99
Q

Who discovered cell cycle check points

A

Ruth Sager

100
Q

Discovering Cell cycle checkpoints Experiment

A

Take normal cell + cancer cell –> Fuse cells –> Get heterokeryon ( have two nuclei) –> get hybridioma

Look several generation later – Look at the phenotype –> Acts more like a normal cell NOT like a cancer cell

LOOK EVEN LATER – look at phenotypes –> now you have cancer cell

Conclusion: Maybe we have genes in system that prevent camcer cells – maybe we have tumor supressor genes

101
Q

Heterokeyron

A

Have cell with two nuclei –> during the fusion process –> have reorganzation of nuclei + chromosome exchange – chromsomes are lost + genes are lost

102
Q

Where is p53 active

A

p53 = active in many checkpoints

103
Q

p53 name

A

Called “guardian of the genome”

104
Q

p53 (overall)

A

Tumor supressor gene

105
Q

p53 action

A

Triggered by DNA damage in G1

p53 = very unstable until it is phosphorylated by a ATMR –> activates p53

When p53 is active = it can do two things:
1. Fix probelm – if few DNA errors = fixes the DNA errors –> cell goes to S phase
2. Kill cell –> if there are many DNA errors = cell goes through apoptosis

***p53 = checks for DNA errors

106
Q

Where were checkpoints first discovered

A

First discovered in Yeast –> budding yeast + Fission yeast

107
Q

Budding yeast Cycle

A
108
Q

Fission yeast Cycle

A

BIOL311 (4 decks)

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