Devo Lect 19 - Apoptosis

Question 2

Critical roles of Apoptosis

Answer 2

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

Question 3

Apoptosis in Circulatory

Answer 3

Pharyngeal arches break down

Question 4

Apoptosis in CNS

Answer 4

Forms the ventricles in the brains for fluid

Question 5

Apoptosis in Immune system

Answer 5

Neutrophils undergo apoptosis after it is done its job

Question 6

Steps (from video)

Answer 6

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

Question 7

Characteristics of apoptosis

Answer 7

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

Question 8

PS

Answer 8

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

Question 9

TUNEL stain

Answer 9

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

Question 10

Why is apoptosis a good way to die?

Answer 10

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

Question 11

C. elegans

Answer 11

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)

Question 12

CED-3 gene

Answer 12

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

Question 13

CED-9 gene

Answer 13

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

Question 14

Why have inhibitors and activators in apoptosis?

Answer 14

More precise control of the process. Very important!

Question 15

Activating apoptosis in C elegans

Answer 15

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

Question 16

BCL2 signaling

Answer 16

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

Question 17

Triggers of Apoptosis

Answer 17

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)

Question 18

Knockouts in T cells

Answer 18

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

Question 19

Define ischemia

Answer 19

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

Question 20

Confusing part of stroke

Answer 20

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

Question 21

Apoptosis vs Necrosis

Answer 21

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

Question 22

Caspases functions

Answer 22

Many involved in apoptosis, some involved in inflammation

Question 23

ICE

Answer 23

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

Question 24

Inflammation in stroke

Answer 24

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

Question 25

Inhibiting caspase 1

Answer 25

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

Question 26

Caspase 1 KO

Answer 26

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