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BIO 3090 > TEST 4 > Flashcards

TEST 4 Flashcards

(68 cards)

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1
Q

G1 phase

A

cell growth

1st phase

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2
Q

S phase

A

cell copies its DNA

2nd phase

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3
Q

G2 phase

A

cell growth

3rd phase

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4
Q

M phase

A

nuclear division/ cell division

4th phase

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5
Q

What sections of the cell cycle/effects are shortened when cell divisions occurs during the embryonic stage?

A

organelles do not grow as big

shortens the G1/G2 phase

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6
Q

Function of cell cycle

A

to prevent incorrect replication of cell

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7
Q

studies of yeast implications on cancer

A

we can study mutations in yeasts cell cycle quickly and relate them to humans as humans have many CDK proteins that are similar to yeasts

this was proven by putting a human CDK into a yeast cell with defective CDKs and the cell successfully divided

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8
Q

CDK and cyclin concentration throughout cell cycle

A

CDK (cyclin dependant kinase protein) levels are constant throughout cell cycle
cyclin levels vary at each stage of the cells life

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9
Q

why do different CDK/cyclin complexes trigger different events

A

each CDK/cyclin complex triggers different events to push the cell forward in its life cycle
different stages require different triggers to progress

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10
Q

Cell cycle check point check list

A

M checklist- is all DNA replicated and is damage repaired
Pull apart chromosomes- Are all chromosomes properly attached to the spindles
S phase- is environment favorable

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11
Q

how does creation/destruction of cyclins progress cell cycle

A

gradual increase comes from transcription of cyclin genes; destruction from targeted destruction

this is to help the cell continue in the cycle- for example Mcyclin & Mcdk destruction pulls the cell out of mitosis- the creation puts it into mitosis

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12
Q

How do cytosol extracts identify cell control systems

A

In an experiment, they took an extract from a rapidly dividing cell in an embryo and put it into a oocyte that was doing nothing, it then instantly started dividing, this taught them the key was in the cytosol

by doing this many times from cells in different stages into an oocyte they were able to identify the components responsible for cell control

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13
Q

how does dephosphorylation trigger cyclin-CDK complexes

A

the creation of these complexes occurs all the time throughout the cell even when the trigger isn’t ready yet

when this occurs the complex is phosphorylated to inactivate the complex, when it is ready it is dephosphorylated which activates the complex immedatly

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14
Q

CDK inhibitors regulating cell cycle

A

CDK inhibitor proteins bind to active cyclin/CDK complexes
once bound it inactivates the complex

this can be done when at each cell cycle checkpoint if the conditions to move on aren’t met - for example, stopping the cell from going into S phase to grow more or when conditions are more favorable

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15
Q

why is G1 to S called start

A

once past this point the cell is committed to completing the cell cycle

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16
Q

why/how are CDK/cyclin complex’s inhibited when entering G1 phase

A

the complexes are deactivated to stop the cell from immedately dividing again, as the cell was full of M cyclin to divide during mitosis

this is done by destruction of all cyclins, stopping synthesis of cyclins, and synthesis of CDK inhibitor proteins

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17
Q

what do cells do when deprived of mitogens

A

they stay in G1 phase or if long enough G0 phase

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18
Q

how does the cell stop before S phase if it has damaged DNA

A

increases activity of P53, transcription regulator
activates coding of inhibitor protein P21 which binds to G1/S-CDKs and SCDKs
this inactivates them, which prevents them from putting the cell into Sphase

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19
Q

What happens if DNA is too damaged to be repaired before S phase

A

P53 activates apoptosis

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20
Q

Whats the difference between terminal differentiation and G0 phase

A

Terminal differentiation is permanent, it cannot continue the cell cycle
G0 phase can continue the cell cycle at a moments notice

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21
Q

what phase(s) vary in length among different types of cells in organisms

A

G1 and G2 phase

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22
Q

Origin recognition complex

A

single protein that sits on the origin of replication in DNA all throughout cell cycle
codes for CDC6 during G1 phase which helps to create a Prereplicative complex

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23
Q

prereplicative complex

A

many different proteins that sit on the origin of replication
waits to activate until an S-CDK is phosphorylates it
once active it begins replicating the DNA
the phosphorylation makes it so that replication of the DNA strand only happens 1
time; this phosphorous is taken off after mitosis

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24
Q

how does incomplete replication cause cellular arrest in the G2 phase

A

M-CDK complexes are not dephosphorylated to drive the cell into mitosis
this is done until correct replication occurs

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25
why is activation of Mitosis extremely quick
when an inactive M-CDK activates by getting dephosphorylated it activates a inactive phosphatase this phosphatase dephosphorylates more M-CDK which acitvates more phosphatases This is a positive feedback loop
26
Cohesins
ties two sister chromatids together
27
Condensins
coils each chromatid into more compact structures
28
contractile ring
during telophase while the cell is being pulled apart into 2 separate cells the contractile ring begins to form in the middle of each cell this contractile ring carries out cytoplasmid division made of actin and myosin
29
mitotic spindles
made of microtubules and motor proteins separates the chromosomes and pulls one into each daughter cell forms in prophase
30
Prophase
condensing of chromosomes | mitotic spindles form
31
Prometaphase
breakdown of nuclear membrane | chromosomes grabbed by mitotic spindles
32
Metaphase
chromosomes line up at center
33
Anaphase
chromosomes get pulled apart
34
Telophase
chromosomes are at poles | contractile ring forms
35
Cytokinesis
cell and cytoplasm is divided by contractile ring into 2 cells
36
Centrosome cycle
duplicated during S phase both are together until mitosis once it begins the 2 centrosomes separate and goes to the opposite ends of the cell the centrosomes begin to create an array of microtubules called an aster
37
kinetochores
where the mitotic spindles attach to on the duplicated chromosome kinetochores recognize the DNA sequnce on DNA that forms a centromere and bind to it, if the DNA is bad the kinetochores wont bind to it and the DNA wont be dispersed properly
38
how does the nuclear envelope breakdown
the lamina, pore proteins and intermediate filaments get phosphorylated and break off into vesicles during prometaphase
39
structure and how spindles attach to kinetochores
kinetochores recognize the DNA sequnce on DNA that forms a centromere and bind to it the kinetochore will bind to an exploratory microtubule linking it to a spindle
40
bi orientation
the fact that the duplicated chromosomes need to be pulled into 2 different directions kinetochores measure tension, if there is slack, the chromosomes will be pulled in 1 direction into 1 cell rather than 2 if that happens the cell will fail to replicate
41
why do chromosomes align at the center in metaphase
the two chromosomes are both attached to 2 different spindles the growing and loss of these 2 spindles/microtubules pull the chromosomes into different directions causing a tug of war. this causes the chromosomes to end up in the middle
42
molecular events in anaphase
in anaphase the 2 chromosomes get pulled apart this is allowed by the cohesin getting destroyed by separase separase is kept inactive by securin until anaphase begins the chromosomes are then pulled by the shrinking microtubules and motor proteins into each cell
43
how does the nuclear envalope reform during telophase
it reforms as the vesicles are released and the proteins lamins and everything are dephosphorylated
44
how do spindles know all chromosomes are attached to kinetechores before pulling the chromosomes apart?
kinetochores that are unattached send a stop signal to the cell cycle control system which inactivates the apc complex, which keeps the chromatids held together
45
Anaphase A
the chromatids are pulled towards the opposite poles, movement is generated mainly at kinetochores
46
anaphase B
the two spindles move apart, this is done by (1) the elongation and sliding of the interpolar microtubules past one another pushing each other apart (2) forces pushing the microtubules at each spindle to pull the poles away from each other towards their own cell cortex
47
when does cytokensis take place
starts during anaphase
48
how is position determined for cleavage furrow
the position is determined by the interpolar microtubules these send out a signal which controls the assembly and contraction of contractile ring which creates the cleavage furrow
49
how are assymetric divisions set up in development
the cell can move its mitotic spindle to an assymetric position creating cells in different sizes, they can also differ in the moelcules inherited which can create different cells
50
how cell change in shape and attachment during life
during proliferation cells have to detatch from one another, usually turning into more circular cells actin gets rearranged
51
cytokensis in plants
enlargement of cell, then an assemply of a wall guided by a phragmoplast made by the old interpolar microtubules at equator form cell wall things are transported there by motor proteins and golgi vesicles
52
how mitochondria is replicated
duplicate by division similar to cell division; present in large enough numbers to be equally distributed when the new cell is formed
53
how ER is replicated
released from the nuclear membrane but remains intact; cut in two during cytokinesis
54
how golgi is replicated
fragmented during M and the fragments associate with the spindle microtubles by motor proteins “hitching a ride!” to the poles
55
3 processes determining body size
balance of | growth division apoptosis
56
how does apoptosis contribute to development
as limbs grow they develop broadly like a spade, but the cell death sculpts the limbs into what they need to be
57
how does apoptosis balance out cell division in healthy liver
with out apoptosis in a liver, the liver will grow unhealthily large apoposis stops this from growing unusally large
58
necrosis vs apoptosis apearance
necrosis- cells explode (1)damages neighbors, inflammation apoptosis- (1) buldges on surface of cell then skrinks then engulfed by another cell (2) recycled
59
how is apoptosis regulated
caspases- enzymes made up of 2 procaspases when a signal is activated to start apoptosis, adapator proteins attach to these procaspases which creates caspase which triggers apoptosis
60
Apoptosis is regulated by proteins
Bcl-2- cell survival by inhibiting release of cytochrome c by inhibiting bax/bak Bax/bak- cell death-releases cytochrome c from mitochondria to cytosol which joins a apoptosome which joins with procaspacse which leads to apoptosis
61
death receptors
Fas- surface receptor which is activated by a ligand which activates a caspace casecade killing the cell
62
proteins influencing cell fate
1- mitogens-stimulate cell division , overcomes intracellular braking mechanisms that block entry into cell cycle in G1 2-Growth Factors- stimulate cell growth (increases size & mass) promotes the synthesis and inhibits degredation of proteins 3-Survival factors- promotes cell survival by suppressing apoptosis
63
how do survival factors regulate neurons in development
cells w/o extracellular signals to reproduce die cells that attach to exess neurons only send growth factors to the neurons they need and deprive the one that they dont which kills them off
64
how do growth factors work in the cell
act through cell surface receptors | turn on intracellular pathways that keep apoptotic program suppressed by regulating Bcl2 proteins
65
mitogens and how they stimulate cell division
Platelet-derived growth factor Hepatocyte growth factor the receptors initate a RTK pathway, stimulates proliferation and healing
66
how growth factors increase size in an organ
increase rate of synthesis and decrease rate of degradation
67
benefits of mitogen/growth factor hybrid
PDGF, stimulating cell growth and progression through cell cycle hybrids are good as they help keep a decent size during growth/proliferation
68
protein that inhibits growth
myostatin-tells muscle when to stop growing, w/o it muscles get fckin huge

BIO 3090 (5 decks)

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