Devo Lect 19 - Apoptosis Flashcards Preview

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Flashcards in Devo Lect 19 - Apoptosis Deck (25):
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Critical roles of Apoptosis

Amphibian metamorphosis; circulatory system; CNS; immune system; limb development

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Apoptosis in Circulatory

Pharyngeal arches break down

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Apoptosis in CNS

Forms the ventricles in the brains for fluid

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Apoptosis in Immune system

Neutrophils undergo apoptosis after it is done its job

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Steps (from video)

Cytochrome C released from mito.; Lipid asymmetry (phosphotidyl serine expressed on outside rather than inside); plamsa membranes become more permeable

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Characteristics of apoptosis

Blebbing of plasma membrane; nucleus and cytoplasm condense; chromatin degrades (nucleases); cytochrome C released from mito membrane, interacts with other molecules, increases intracellular Ca; PS exposed on plasma membrane; membrane is more permeable; cell fragmentation

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PS

Phosphotidyl serine; usually involved in cell signaling. When exposed on outside it acts as a marker for macrophages

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TUNEL stain

stain that binds to cut up DNA, adds a labeled nucleotide to the end of the fragments; more fragments results in more colour

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Why is apoptosis a good way to die?

Doesn’t release DNA and lysosomes (although they don’t work at normal pH), less inflammation; DNA is foreign to immune system, could cause autoimmune response

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C. elegans

1090 cells in fate map, only 959 survive - apoptosis; tested with mutagens, see if cells undergo apoptosis more or less (by number of mutant cells)

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CED-3 gene

CED-3 in C. elegans: mutant, 1090 cells (no apoptosis), overexpressed = apoptosis; inducer; mammal homologue = caspase

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CED-9 gene

in C. elegans; mutant increase apoptosis, overexpression = less apoptosis; inhibitor of CED-3

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Why have inhibitors and activators in apoptosis?

More precise control of the process. Very important!

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Activating apoptosis in C elegans

EGL-1 (death signals) inhibit CED-9, so CED-9 can not inhibit CED-3 and apoptosis starts

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BCL2 signaling

CED-9 homologue in mammals; in intracellular membranes (eg mito.). Inhibits Apaf1 which activates Caspase 9; BCL2 inhibited by Bax and Bik, which also form a pore in the mito to release cytochrome C; cyto C binds to Apaf1 and initiates apoptotic pathway

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Triggers of Apoptosis

Killer T cells; kill infected cells. Steps: 1. recognize viral antigen, 2. Release of cytolytic granules from T cell (proteases, nucleases, perforin (pores)), 3. Fas ligand (on T cell) and receptor trigger apoptotic cascade (caspases)

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Knockouts in T cells

FasL -/- : decrease effectiveness of apoptosis initiation by 50%; FasL and Perforin -/- : cannot kill cells at all

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Define ischemia

Lack of oxygen in a tissue due to a block of a blood vessel, resulting in cell death - necrotic

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Confusing part of stroke

Initial cell death due to ischemia, but then other cells around it continue to die around it after the stroke.

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Apoptosis vs Necrosis

Apoptosis is programmed, good because you don’t release materials out; necrosis is death in response to damage or chemicals etc., spills contents all over

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Caspases functions

Many involved in apoptosis, some involved in inflammation

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ICE

Interleukin converting enzyme: aka caspase1, cuts part of IL to activate it. Interleukins stimulate inflammation

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Inflammation in stroke

Increased inflammation in brain due to initial stroke, some cells die in response to this

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Inhibiting caspase 1

Induce stroke and use Caspase 1 inhibitor; much less cell damage, and much less IL present; lots of drug research to treat with these w/o direct injection to brain

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Caspase 1 KO

when exposed to oxygen glucose deprivation (OGD), WT has huge increase in IL; in KO, much lower. Ischemia treatment: WT has high caspase 9; KO has much lower; 50% less damage