Peroxisome, Mitochondrion, Lysosome

Front 1

How would you see peroxisomes in a slide in regards to diaminobenzidene plus H2O2

Back 1

Stain: clear vesicles become super dark (catalase is precipitated)

Front 2

What kind of membrane does peroxisome have?

Back 2

Lipid membrane

Front 3

Explain how myelin is formed with peroxisomes

Back 3

Metabolic: Glycerol enters peroxisome, plasmolygen is released, important in the formation of myelin

Front 4

Is fat made or burned in the peroxisome?

Back 4

Burn, baby burn

Front 5

Explain Peroxisome transport signal 1 (what is the aa CODE?)

Back 5

Cargo binds with signal...

Any protein at the C-terminal with a serine-lysine-leucine at the beginning is the code to bind with peroxisome protein "5", which interacts with all the other peroxisome proteins in order to release PTS1 into the peroxisome

Front 6

Explain PTS2. Is it more or less conserved?

Back 6

Code on the n-terminal which binds with "7" same shuttle system. Less conserved

Front 7

PPAR-where do the live, how do they work? Use the components of RXR, FABP, etc.

Back 7

Peroxisome proliferating activation receptors: proteins that live in nucleus.

Form complex with RXR (bind with retinoic activating receptor), these two bind with DNA (Peroxisome proliferating response element) makes DNA downstream

In order to turn onto gene, free fatty acids with fatty acid binding protein, which reacts with PPAR, which binds with RXR, which reacts with DNA

Front 8

PPARs in the skeletal muscle: what do PPARdeltas cause in terms of glucose/lipid oxidation? What real life activity stimulates it? Short/long term fasting, age, diabetes...how is it affected?

Back 8

Interacts with mitochondria to cause REDUCED GLUCOSE oxidation and INCREASE LIPID OXIDATION
Exercise
PPARdelta goes up with exercise
Short term fasting: rise
Long term fasting: drops
Age: older:: drops
Diabetes: drops

Front 9

X-linked adrenoleukodystrophy--what's goin on here?

Back 9

Very long chain fatty acids in blood are increased

Mutation in ABCD1 gene (mutation in ATP dependent transporter of fatty acids into peroxisome)

Fatty acid builds up in cytosol, in blood, knock out adrenal glands, not being broken down in peroxisome

Front 10

What are the different components of the mitochondria?

Back 10

Matrix, inner membrane, outer membrane, intermembrane space, crista

Front 11

Where are there excessive protons in the mitochondria? How is ATP synthase involved?

Back 11

Space between inner and outer mitochondrial membrane (result of electron transport chain), in the intermembrane space

ATP synthase: allows hydrogen ions to flow back into the matrix, cross the membrane:: as it passes through, mitochondria uses energy to pump ADP and phosphate into ATP

Front 12

How are ATP synthesis and ATP hydrolysis different with ATP synthase?

Back 12

ATP synthesis: hydrogens pass through synthase, rotorary handle rotates, ATP is pumped out of mitochondria,

ATP hydrolysis: hydrogen ions are put out, rotorary handle is turned opposite direction, ATP is used to pump H out (becomes ADP)

Front 13

Are mitochondria always one shape?

Back 13

No--they can go through fission (DRP dynamin related protein) or fusion (optic atrophy) from bigger to small mitochondria (DNA throughout mitochondria)

equilibrium

Front 14

Is mitochondria DNA circular or linear?

Back 14

Circular

Front 15

Lysosomes deal with garbage...

Also, do lysosomes have a membrane?

Back 15

Proteins that are broken, damaged, etc.

Transported is regulated (coded)

Yes, they have a membrane and a whole bunch of garbage inside of it (similar to autophagosome, but prolly never see that on a microscope)

Front 16

How does the lysosome get its low pH?

Back 16

Hydrogens are pumped into the luen of the lysosome (acid hydrolases in the lysosome need acidic envrionment)

Front 17

What is proprotein processing? What protein is it associated with for lysosomes? What other characteristics are associated with that protein?

Back 17

Proprotein: pro domain which is cleaved off before they're active

associated with Hydrolases

Bulk degradation, antigen processing, ECM degradation, initiation of apoptosis

Front 18

What are LMPs?

Back 18

Lysosomal membrane proteins (protein import, transport of degradation fo products to cytoplasm

Front 19

How are early endosomes related to lysosomes? Where does it receive vesicles from? What happens to the cargo?

Back 19

Early endosomes receives incoming endocytic vesicles (from transgolginetwork) sorts for recycling and degradation

Cargo-fuses to become late endosome, which becomes a multivesicular body fused with lysosome to degrade everything inside of it (endolysosome, can't tell if it's late endo or lyso)

Front 20

What is the major site where cargo destined for recycling is sorted form cargo en route to late endosomes and lysosomes?

Back 20

Early endosomes

Front 21

How are early endosomes subdivided?

Back 21

-into the globular vacuolar or sorting endosome
-associated tubules indicated as "recycling tubules"--these go back up to the surface to gather vesicles

Front 22

Does the TGN ever communicate with anything other than the early endosome or the surface (that is later picked up by early endosome?)

Back 22

Yes-vesicles can be sent directly to the late endosome/multivesicular body (sorted there as well, cargo proteins recycle to TGN)

Front 23

What happens to cargo not destined for recycling? How does ILV come into play?

Back 23

Requires active sorting into late endosomes, mediated by inclusion into INTRALUMINAL VESICLES (ILV)--which segregate ligand-receptor complexes from the cytoplasm, terminating their signaling (involves ubiquitination)

Front 24

Describe how the network works, from golgi to early endosome, of transportation of a cargo, with lysosomal hydrolase and mannose

Back 24

Proprotein lysosomal hydrolase precursor and mannose ships over to next layer of Golgi, p-GLCnAC is added, shipped over to next layer, P0GLcNAc is removed:: mannose becomes mannose6phosphate, binds to M6Preceptor, little vesicle is formed with clathrin coat, targeted for release to the early endosome, enters lumen of endosome (acidic) allows protein receptor to come off complex


Anything with mannos6phosphate will be targeted and sent to endosome

Front 25

Explain late endosome to lysosome with its enzymes and hydrolytically active, low pH compartments

Back 25

Enzymes in late endosome becomes high concentrations in lysosome (enzymes of lysosome will fuse with late endosome to have even more enzymes)

Enzymes are active very precisely in the process

Front 26

What are the different entry ways to lysosome?

Back 26

Endocytosis (early endosome to late endosome to lysosome)

Phagocytosis (bacterium from extracellular fluid into cytosol, becomes phago some, goes to lysosome

Autophagy (times of starvation) organelles with membranes around them get shipped to lysosome

Front 27

What is the primary function of lysosomes

Back 27

Hydrolyze all macromolecules to monomeric subunits and recycle subunits via transmembrane transport to cytoplasm (important during postnatal starvation)

Front 28

Are lysosomes acidic or basic? How does it maintain that environment?

Back 28

Acidic
Pumping of H+ ions in using vacuolar H+ATPase

Front 29

Is there diffusion in the lysosome?

Back 29

NO, in or out, completely walled off

Front 30

What happens to the pH levels in the different organelles?

Back 30

Golgi-6.7to 6.0 cis to trans
Secretory vesicles are 5.5
Early endosome is about 6.5
Late endosome is less than 6
Lysosome is less than 5.5, closer to 4.5

Front 31

What do they mean by lysosomal "storage" diseases? Where in the body are they first presented?

Back 31

Because macromolecules cannot be broken down, they build up and is stored in the lysosome, causing an increase in the cell, which causes a lot of problems.

They usually present themselves as neurological defects (brain is affected first)