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


Apoptosis in Circulatory

Pharyngeal arches break down


Apoptosis in CNS

Forms the ventricles in the brains for fluid


Apoptosis in Immune system

Neutrophils undergo apoptosis after it is done its job


Steps (from video)

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


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



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


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


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


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)


CED-3 gene

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


CED-9 gene

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


Why have inhibitors and activators in apoptosis?

More precise control of the process. Very important!


Activating apoptosis in C elegans

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


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


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)


Knockouts in T cells

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


Define ischemia

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


Confusing part of stroke

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


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


Caspases functions

Many involved in apoptosis, some involved in inflammation



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


Inflammation in stroke

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


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


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