module 11 Flashcards

1
Q

question: how is apoptosis a part of sculpting digits?

A
  • week 6 of dev. = skin webbing between digits
  • week 11 = webbing gone
  • skin is gone bc apoptosis
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2
Q

question: what does a TUNEL assay do?

A
  • see nicks/DNA breaks in DNA
  • dUTP is incorporated into nicks by adding enz.
    ⤷ deoxynucleotidyl transferase
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3
Q

question: how is apoptosis involved w/ frogs?

A
  • tadpole goes through metamorphosis to become frog
  • apoptosis removes tadpole tail
  • apop. stim. by thyroid hormone in blood

**similar tail loss happens in humans

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4
Q

question: how is apoptosis involved in nervous system?

A
  • normal brain only needs 1/2 of the neurons originally produced
  • cells that don’t achieve synaptic connections get cell death
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5
Q

question: how can cell death be bad in the human body? (4 ex.)

A
  • inappropriate cell death -> disease
  • ex. alzheimer’s
    ⤷ neurons in hippocampus region die
  • ex. huntington’s
    ⤷ neurons in striatum die
  • ex. parkinson’s
    ⤷ dopamine neurons in substantia nigra die
  • ex. duchenne muscular dystrophy
    ⤷ muscle cells atrophy
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6
Q

question: what are the ways in which a cell can die? (2) + define them

A
  1. necrosis
    ⤷ cells swell and release contects into surrounding tissues
    ⤷ bad (can lead to infection)
  2. apoptosis
    ⤷ disposal of cellular debris that doesn’t damage surrounding cells
    ⤷ from stress, damage, or normal development
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7
Q

question: what are the steps of the apoptotic pathway? (3)

A
  1. execution
  2. engulfment
  3. clearance
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8
Q

explain: process of apoptosis

A
  • chromatin condenses
  • nuclear envelope breaks down
  • nucleus contents = fragmented
  • DNA broken down
  • cell mem. blebs
  • makes compartments each filled w/ debris from dead cell
  • each fragment gets phagocytized
    ⤷ reused and recycled
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9
Q

question: what is blebbing?

A
  • creating protrusions or bulges as the cell shrinks
  • happens to cell mem.
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10
Q

question: why c.elegans good for apoptosis studies?

A
  • know there are 947 somatic cells
  • can tell that exactly 131 cells undergo apoptosis
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11
Q

question: how were c.elegans studied for apoptosis?

A
  • used assay to ID muts. in genes required for apop.
    ⤷ cell death genes = ceds
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12
Q

question: what is the effect of ced-1 on cell death in c.elegans

A
  • loss of func. mut. in ced-1 leads to apop. but cells not engulfed by phagocytosis
    ⤷ so they stay and researchers can study
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13
Q

question: is ced-3 important in apop.? what if there’s a mut. in ced-3?

A
  • mut. in ced-3 -> no apoptotic genes
  • if ced-3 not functional, no apotosis can take place
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14
Q

name: genes required for apop. in c.elegans?

A
  1. ced-3
  2. ced-4
  3. ced-9
  4. egl-1
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15
Q

question: what is the human homologue for the c.elegans genes?

A
  1. ced-3 = caspase-9
  2. ced-4 = apaf-1
  3. ced-9 = Bcl-2
  4. egl-1 = Bid, Bim, Bad
    ⤷ Bid reg. Bak
    ⤷ Bim reg. Bax
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16
Q

question: what does each gene do in c.elegans apoptotic pathway?

A
  • ced-3 and ced-4 form complex = caspase holoenz.
    ⤷ targets diff. prot. for degradation
  • ced-9
    ⤷ inhibitor of apop.
    ⤷ inhibit activation of the caspase holoenz.
  • EGL-1
    ⤷ sig. for apop. that activates pathway
    ⤷ inhibits ced-9
17
Q

explain: results if caspase holoenz. or ced-9 had a mutation

A
  • ced-3 ced-4 complex
    ⤷ no apop.
  • ced-9
    ⤷ all cells die
18
Q

question: what does the caspase holoenz. do?

A
  • protease activity
  • prot. degradation
  • cell death
19
Q

question: how is the caspase holoenz. activated (formed)?

A
  • ced-9 is inhibiting by binding to ced-4 dimers
  • adding egl-1 inhibits ced-9 to release ced-4
  • ced-4 binds to 3 and forms caspase holoenz.
  • formation -> activation
20
Q

question: what is the role of mito. in apop.?

A
  • ced-9 prot. (Bcl-2) is on surface of mito.
  • prot. on mito mem. changes it’s permeability
21
Q

question: what do Bad and Bax do (cytochrome C)?

A
  • apoptotic sig. = Bad
  • Bad = inactive until dephosphorylated
  • Bad binds to Bcl-2 -> activation of Bax (another ced-9 prot.)
  • Bax aggregates and forms pores that increase permeability and release mito. into cytosol
  • also releases cytochrome C
22
Q

question: how does trophic factor removal lead to apop.?

A
  • trophic factors prevent apop. (initiate kinase cascade to phosphorylate Bad)
  • removing trophic factors -> Bad can be dephosphorylated -> apop.