Module 11 Flashcards

(38 cards)

1
Q

How can dUTP be incorporated in the nicks of apoptotic cells? (TUNEL assay of digit development)

A

by the addition of terminal deoxynucleotide transferase enzyme which allows for the detection of cells undergoing apoptosis

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2
Q

what does an increase in thyroid hormone do to frogs?

A

this induces metamorphosis that occurs in the tails that are induced to disappear

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3
Q

why do some nerve cells survive and others don’t?

A

only certain cells receive sruvival factors, those who do not undergo apoptosis

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4
Q

how many neurons originally produced in the brain must undergo apoptosis?

A

half of the original cells

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5
Q

what cells in the brain must undergo apoptosis?

A

I) cells that have faulty connections

II) cells that have not achieved a synaptic connection

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6
Q

true or false: the number of nerve cells match the number of target cell?

A

true

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7
Q

What are the results of TOO much cell death?

A

neurodegenerative disorders

  • alzheimers (hippocampus + cerebral cortex)
  • huntingtons (striatum)
  • parkinsons (dopamine neurons in substantia nigra)
  • DMD (muscular degeneration)
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8
Q

Describe necrosis

A

during this process cells swell up and release its content in nearby tissue which may lead to infection and is potentially dangerous

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9
Q

Describe apoptosis

A

this is PROGRAMMED cell death, the cell disposes of its cellular debris and does so without causing damage to the surrounding cells, the contents are rather contained and recycled by surrounding cells
Apoptosis works by execution, engulfment and clearance of its cellular debris

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10
Q

what visible changes appear in the cell during apoptosis?

A
  1. the cell gets smaller
  2. blebbing occurs: protrusions/bulges appear in the cell
  3. the mitochondria lose permeability
  4. nucleus breaks down into vesicles which will be phagocytized
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11
Q

how many somatic and apoptotic cells can be seen in C elegans

A

947 somatic cell

- 131 cells undergo programmed cell death

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12
Q

what does a mutation in the ced-1 gene of C. elegan do?

A

the ced-1 gene usually allows the cell to undergo apoptosis

a mutation in this gene, the cell still undergoes apoptosis but lacks the ability to engulf cells by phagocytosis

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13
Q

what does a mutation in the ced-3 gene of C. elegan do?

A

with a ced-1 and ced-3 mutation NO APOPTOSIS occurs

the ced-3 gene is said to be essential for the apoptotic pathway

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14
Q

what 4 genes are essential for the apoptotic pathway?

A

I) Ced-3
II) Ced-4
III) Ced-9
IV) Egl-1

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15
Q

what are the human homologs of the Egl1 protein?

A

Bid and Bim, they are part of the BH3 family of proteins

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16
Q

what is the Bcl2-protein

A

this is the human homolog of Ced-9 nad is bound to the mitochondrial membrane, it is in control of related proetins: Bak and Bax

17
Q

what is the caspase holoenzyme?

A

a complex formed between ced-4 and ced-3 proteins

it is a protease that targets a variety of proteins

18
Q

what time of mutations prevent apoptosis?

A

loss of function mutations in ced-3 or ced-4

19
Q

what happens in a loss of function mutations in ced-9?

A

all of the cells die by inhibition of the caspase holoenzyme

20
Q

what happens in a loss of function mutation in ced-3 or ced-4?

A

apoptosis is prevented

21
Q

how does Egl-1 signal apoptosis?

A

by inhibiting the inhibitor (ced-9) it is able to induce the apoptotic pathway

22
Q

what do we call the human version of the caspase holoenzyme?

A

the apoptosome, it contains direct homologs of the ced-4 (Apaf1) and ced-3 (Caspase-9)
both the function of the apoptosome and the caspase holoenzyme lead to cell degradation and cell death

23
Q

how does ced-9 inhibit apoptosis?

A

by binding to ced-4 dimers and keeping them inactive

24
Q

how is ced-4 released?

A

by Egl1 binding to Ced-9, once released ced-4 binds to ced-3 to form the caspase holoenzyme

25
What human homolog alters mitochondria permeability?
Bcl2
26
What does the inactivation of Bcl2 do?
this creates pores in the mitochondria, making it more permeable, this process is associated with apoptosis
27
when is the Bad protein inactive?
when phosphorylated Bad is inactive and bound to protein 14-3-3
28
what happens is Bad protein is dephosphorylated?
in this case it is activated and released from the 14-3-3 protein, it can now bind to Bcl-2 protein
29
true or false: the activation of Bax leads to activation of Bcl-2?
false, in fact the activation of Bcl-2 leads to the activation of Bax
30
what creates pores in the mitochondrial membrane?
clusters of Bax protein accumulate on the mitochondrial membrane to create pores and increase permeability during apoptosis
31
what proteins are released from the mitochondria?
the cytochrome c protein
32
what is the use of cytochrome c?
it is an essential protein for the formation of the mammalian apoptosome
33
What leads to apoptosis?
intrinsic cell damage, such as; DNA damage of cellular stress or extrinsic cellular (pro-apoptotic) signals
34
true or false: apoptotic signals promote Bad protein phosphorylation
false, apoptotic signals promote Bad protein de-phosphorylation, since bad is inactive WHEN phosphorylated
35
what may keep the cell alive? and how?
trophic factors, by initiation a kinase cascade that leads to the phosphorylation of the Bad protein keeping it inactive
36
what happens if trophic factors are removed?
Bad is dephosphorylated and activated leading to a cascade of events that result in cell death
37
how many cells die per day in the average human?
50-70 billion
38
true or false: apoptotic pathways are conserved throughout bacteria and mammals
true