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cellular growth regulation Flashcards

1
Q

define hyperplasia

A

an increase in cell numbers

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2
Q

define hypertrophy

A

an increase in cell size

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3
Q

what are the main stages of cell division

A

cell cycle stages (G1, S, G2 and M)

one stage outside of cell cycle

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4
Q

what are restriction points (in cell cycle)

A

checkpoints at which a cell will exit the cell cycle if certain requirements to proceed to synthesis are not met

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5
Q

what is apoptosis

A

programmed cell death
coordinated method of cell dismantling - & eventually phagocytosis
occurs in response to DNA damage and viral infection.

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6
Q

briefly, what do cytokines and interlukins do

A

some stimulate proliferation of cells and maintain their survival
some stimulating differentiation of cells and inhibit proliferation
some induce apoptosis

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7
Q

what do mitogens do

A

stimulate cell growth

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8
Q

what are the 3 broad classes of hormones

A
  1. p aracrine
  2. autocrine
  3. endocrine
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9
Q

what are paracrine hormones

A

hormones produced locally to stimulate proliferation of a different cell type (in nearby environment) that has the appopriate cell surface receptor

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10
Q

what are autocrine hormones

A

hormones produced by a cell that also expresses the appropriate cell surface receptor

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11
Q

what are endocrine hormones

A

hormones released into circulation for distant effects e.g. IGF-1

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12
Q

what happens to cells in culture when you add growth factor

A

stimulate cell growth of the population

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13
Q

what happens when you remove growth factor from cells in culture

A

population will undergo growth arrest as they require continuous stimulation to grow.

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14
Q

what happens when you add a growth inhibitor such as TGFb to cells in culture

A

cause growth arrest of cells

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15
Q

what happens when you add TNFa to cells in culture

A

cause cell death

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16
Q

what are the phases of the cell cycle

A

Interphase is composed of G1 phase (cell growth), followed by S phase (DNA synthesis), followed by G2 phase (cell growth). At the end of interphase comes the mitotic phase, which is made up of mitosis and cytokinesis and leads to the formation of two daughter cells

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17
Q

what happens during G1 of cell cycle

A

the cell grows physically larger, copies organelles, and makes the molecular building blocks it will need in later step

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18
Q

what happens during S stage of cell cycle

A

ell synthesizes a complete copy of the DNA in its nucleus. It also duplicates a microtubule-organizing structure called the centrosome. The centrosomes help separate DNA during M phase

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19
Q

what happens during G2 of cell cycle

A

he cell grows more, makes proteins and organelles, and begins to reorganize its contents in preparation for mitosis.

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20
Q

what happens after interphase in cell cycle

A

cell can either come out of cell cycle - into G0. (cells undergo growth arrest)
or undergo mitosis

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21
Q

what may cause cells in G0 to reenter cell cycle

A

at this phase cells are sensitive to growth factor.

exposure to GF = reenter cell cycle.

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22
Q

what is DNA content of the cell after S phase

A

4N

replicating its DNA

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23
Q

what is DNA content of the cell after dividing

A

2N

diploid

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24
Q

how do we measure the stage of cell cycle

A

use a fluorescence activated cell sorter

this measures amount of flourescence in a cell based on how much DNA it has.

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25
how does a population of cells with a low rate of cell division present on cell sorting
most of cells in g1 phase | only few are in S or G2/M phase
26
how does a population of cells with a high rate of cell division present on cell sorting
much more of cells in s and G2/M phase | which explains why pop is growing a lot
27
what does it mean when we say DNA is replicated semiconservatively
the daughter cells containing one parental strand and one new strand.
28
in which direction is new DNA sythesised and by which enzyme
5' to 3' direction by DNA polymerase
29
in which direction is DNA read
read in 3' to 5' direction
30
what safegaurds does DNA have to guard against mutation
proof-reading function and mismatch repair system
31
why do we have the formation of okazaki fragments
DNA polymerase only works in the 5'-3' direction so on laying down primar from replication fork: one strand is able to be made continuously other strand has to keep reinitiating sythesis of the strand by laying down new primers.
32
what do we do with the okazaki fragments
is called the discontinuous strand. | the fragments have to be ligated together after removal of RNA primers
33
what are the 5 stages of mitosis
1. prophase 2. prometaphase 3. metaphase 4. Anaphase 5. telophase
34
what happens in prophase
- nuclear membrane breaks down (nucleus less definite) | - mitotubular spindle apparatus assembles with centrioles migrating to opposite poles of nucleus
35
what happens in prometaphase
- nuclear membrane completely breaks down | - kinetochores of chromosomes attach to spindle
36
what happens in metaphase
- chromosomes align in equatorial plane
37
what happens in anaphase
sister chromatids separate and migrate to opposite poles of the cell
38
what happens in telophase
Daughter nuclei start to form
39
what happens in cytokinesis
- Division of cytoplasm between cells | - Chromosomes decondense back to chromatin
40
what effect does 5-flourouracil have on the cell cycle
5-fluorouracil (an analogue of thymidine) blocks thymidylate
41
what effect does bromodeoxyuridine
analogue of thymidine - incorporated into DNA detected + detected by antibodies detected by antibodies to identify cells that have passed through the S phase
42
what effect does colchicine have on the cell cycle
stabilises free tubulin preventing microtubule polymerisation and this arrests the cell in mitosis - used in karyotype analysis
43
what effect does paclitaxel (Taxol) have on the cell cycle
stabilises microtubules preventing de-polymerisation, inhibiting their function
44
where are the three restriction points of the cell cycle
1 - late G1 2 - just before entry into meiosis 3 - at the point where chromosomes are aligned on equatorial plate spindle
45
what does the late G1 checkpoint asess
Is DNA damaged what is the cell size has it grown adequately are their sufficient metabolite/nutrient stores
46
what does the post entry into meiosis checkpoint assess
Is the DNA completely replicated | Is it damaged
47
what does the checkpoint at the point where chromosomes are aligned on the equatorial plate spindle assess
are all the chromosomes aligned
48
at which point of cell cycle are cells most responsive to growth factors
g1
49
at what stage are cells in a tissue regulated
G1
50
what are kinases
enzymes that phosphorylate other proteins
51
what is the active kinase made up of
1 - CDK calatytic unit | 2 - cyclin regulatory unit
52
what is a cyclin dependent kinase
requires the binding of cyclin to phosphorylate | involved in regulating the cell cycle
53
where does cyclin bind on the cyclin dependent kinase
cyclin binds to CDK to form the active cyclin CDK complex | is then able to phosphorylate
54
how do we regulate the cyclin-CDK activity
1 - through cyclin synthesis + degredation (via proteosome) 2 - post-translational modification by phosphorylation. site of phosphorylation = activation/inhibition or destruction 3 - dephosphorylation of the complex 4 - binding of cyclin dependent kinase inhibitors
55
what is the role of retinoblastoma in inhibiting progression through cell cycle
RB = key substrate of G1 & G1/S CDK. RB is usually unphosphorylated. when in this state, it binds to E2F. bound so E2F cannot stimulate S-phase proteie expression so cell cannot progress into S phase.
56
role of CDK + retinoblastoma in progression into S phase.
When CDK present, it phosphorylates E2K so RB released. E2K -> nucleus. binds promoter regions of cyclin and S-phase proteins. -> Production of these S phase proteins allows for DNA replication of the S phase to start
57
what are some cyclin dependent kinase inhibitors
two families of CDKIs 1 - CDK Inhibitory Protein/Kinase inhibitory protein family 2 - Inhibitor of Kinase 4 family
58
why do we need CDK inhibitors in the body
Loss of some of these CKIs can lead to cancer as no brake on progression.
59
how do CDK Inhibitory Protein/Kinase inhibitory protein family work
- protein inhibitors act on both sides of catalytic unit and cyclin subunit - can inhibit all other CDK-cyclin complexes (late G1, G2 and M) so can work throughout the cell cycle
60
what stimulates the expression of | CDK Inhibitory Protein/Kinase inhibitory protein family
weakly by TGFb (inhibitor of cell growth) and strongly by DNA damage (by TP53)
61
what stimulates Inhibitor of Kinase 4 family
stimulated strongly by TGFb
62
what does Inhibitor of Kinase 4 family inhibit
Specifically inhibit G1 CDKs (e.g. CDK4, the kinase activated by growth factors)
63
how do growth factors induce cyclin expression
1.GF binds to cell surface receptor, triggering signal transduction 2.1st wave of transcription/translation products go back to nucleus. stimulate delayed gene expression Initial proteins are cyclin D and CDK proteins & E2F 3.Cyclins stimulate further expression of cyclin 4.E2F inactive, as is bound to unphosphorylated RB 5.Cyclin-CDK complex increase. More phosphorylation of RB .’. E2F release 6.Expression of E2F responsive genes that allow progression into S phase
64
what happens if DNA damage is detected at a restriction site?
1. CDKI arrest the cell cycle 2. cell attempts to repair DNA damage by nucleotide excision enzymes or mismatch repair system 3. if repair is excessive/irreparable, triggers apoptosis (via BCL2 family & caspases)
65
what is p53
is a transcription factor. | exists transiently in the cell and degraded by enzymes
66
role of p53 in respnse to DNA damage
if DNA damage is detected: P53 phosphorylated = more stable 1. stimulates expression of CDKI (.'. arrests cell cycle) 2. P53 stimulates expression of DNA repair proteins (if repaired cell -> cell cycle) 3. if repair not possible, p53 stimulates apoptosis

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