Exam #1: Cell Biology IV Flashcards
(47 cards)
1
Q
How are phospholipids synthesized?
A
- Phospholipids are synthesized on the cytosolic monolayer
- Scramblase flips the phospholipids into the other monolayer, maintaining symmetry
2
Q
Scramblase
A
- Flips phospholipids from on monolayer into another
- Maintains membrane monolayer symmetry
3
Q
What happens when additional plasma membrane is no longer needed?
A
Macroautophagy
4
Q
Phospholipid Exchange Protein
A
transfers phospholipids from the ER to another membrane in the cell
5
Q
What is Atlastin?
A
- GTPase that is involved in constructing & shaping the ER
- ER scaffold protein
6
Q
Atlastin Abundance
A
Increased ER membrane fusion & absence of Golgi
7
Q
Atlastin Deficiency
A
- ER becomes fragmented
- Hereditary Spastic Paraplegia
8
Q
Hereditary Spastic Paraplegia
A
- Caused by Atlastin deficiency
- Leg stiffness, gait disturbances, facial dysmorphia
9
Q
Proteasome
A
- In BOTH cytosol & nucleus
- MOST are ubiquitin dependent, but NOT all
- Energy dependent
10
Q
What are examples of things that are eliminated by proteasomes?
A
- Cyclin/CDKs (mitotic factors)
- CFTR
11
Q
What disease states inhibit proteasome action?
A
- Prion proteins (Creutzfled Jacob Disease)
- Amyloid (Alzheimer’s Disease)
- Lewy Bodies (PD)
12
Q
Bortezomib
A
- Proteasome inhibitor that is used in the treatment of multiple myeloma
- Decreases the degradation of pro-apoptotic factors i.e. causes an elevation of pro-apoptotic factors
13
Q
Golgi Apparatus
A
- Situated near the nucleus
- Contains cisternae (sacs)
14
Q
What are the functions of the Golgi Apparatus?
A
- Sorting proteins from the ER
- Protein modification
- Packaging of proteins into vesicles
- Movement of proteins through membranous compartments of the cell
15
Q
Wilson’s Disease
A
- Defective copper transporter, ATB7B
- Causes a decrease in plasma ceruloplasmin
- Defective excretion of copper
- Copper is neurotoxic & also accumulates in the cornea
16
Q
ATB7B
A
- Copper transporter that is embedded in the membrane of the Golgi
- Allows for movement of copper into the Golgi
- Also, allows for movement of copper into secretory vesicles that are eliminated in the bile
17
Q
Ceruloplasmin
A
- Major copper-binding protein in the blood
- Binds copper in the Golgi apparatus & then excreted into the blood
18
Q
Apoceruloplasmin
A
Copper not bound to binding protein
19
Q
Kayser-Fleischer Ring
A
- Copper deposition in the cornea
- Sign of Wilson’s Disease
20
Q
Dysferlin
A
- Microperforations occur in muscle cells during muscle activity
- Dysferlin protein is involved in “patching”
- Packaged in the Golgi
- Mutated in some forms of Muscular Dystrophy
21
Q
Proinsulinemia
A
Normal:
- Pre-proinsulin is packaged & sent to the Golgi
- Golgi converts pre-proinsulin into proinsulin
- Golgi then packages proinsulin w/ enzyme that will cleave proinsulin into insulin
- Regulated Pathway
Pathologic:
- Proinsulin is mutated & missorted into the constitutive pathway
- Proinsulin converting enzyme is sorted into Regulated Pathway
- Misorting leads to an increase in proinsulin, proinsulinemia
22
Q
Negative Golgi Image
A
- Light stained region next to the nucleus
- Cytoplasm is basophilic, but Golgi is not
- Gives negative image
23
Q
Positive Golgi Image
A
- Golgi stained with heavy metal
- View electron dense profiles
- In nerve, Golgi encircles the nucleus
24
Q
Cis Golgi Network
A
Receives vesicles from the ER
25
Trans Golgi Network
Secretes vesicles
26
Endosomal Compartments
- Near the cell membrane
- Early & recycling endosome
- Multivesicular Body
- Late endosome
27
Lysosomal Compartments
- Close to the interior of the cell
| -
28
Early Endosome
- Located in the cell's periphery
| - pH 6.2-6.5
29
Recycling Endosome
- Just beneath the plasma membrane
- Store membrane proteins e.g. glucose transporters
- Insulin binding, insert glucose transporters into the plasma membrane
30
Multivesicular Body
- Deeper than early endosome
- Budd off the early endosome
- Transported along microtubules to late endosome
- pH 5.0- 6.2
- Origin of exosomes
31
Late Endosome
- Fuse with multivesicular bodies
- pH ~5.0
- Fuse with or mature into lysosomes
32
What controls the acidity of the endosomal and lysosomal compartments?
H+-ATPase
33
Fates of Endocytosed Receptors & Ligands
- Receptor is recycled & ligand is degraded- LDL
- Receptor & ligand are recycled- Transferrin
- Receptor & ligand are degraded- EGF
- Receptor & ligand are transported across cell & secreted (transcytosis)- IgA (secretory antibody)
34
What uncouples receptors & ligands when the receptor is recycled and the ligand is not?
Acidic pH of the early endosome
35
Achondroplasia
- Dwarfism
- Caused by abnormal recycling of the FGFR3 (fibroblast growth factor receptor) back to the surface of the cell
- Overstimulates & amplifys the signal, which ultimately leads to dwarfism
36
Transport of Lysosomal Hydrolases
- Lysosomal Hydrolase Precursor is tagged with mannose
- Cis-->Trans Golgi
- Mannose 6-phosphate receptor recognizes the mannose tag
- Delivered to endosome or lysosome
37
At what pH are lysosomal hydrolases most effective?
Low
38
What are the different pathways used to degrade material?
- Autophagic
39
What are the different autophagic processes?
1) Macroautophagy (organelles)
| 2) Microautophagy (protein)/ Chaperone-mediated autophagy
40
Heterophagosome
- Contains something that was brought in from the external environment to be degraded
- vs. autophagosome
41
Heterophagolysosome
- Heterophagosome fused with lysosome
| - Secondary lysosome
42
Residual Body
- Material that could not be digested by the lysosome
| - Forms lipofuscin
43
What is special about osteoclasts?
Secrete lysosomal hydrolyses for degradation of bone material
44
Primary Lysosome
- Not degrading anything/ has not received a phagosome
| - Homogenous
45
Secondary Lysosome
- Fused with phagosome
- Degrading material
- Heterogenous (light & dark)
46
Pompe Disease
- Caused by a defect in the delivery of the lysosomal hydrolases to the lysosome
- Glycogen storage disorder, where glycogen accumulates in lysosomes
47
Tay-Sachs Disease
- Deficiency in the enzyme that breaks down sphingolipids
- Lipid material accumulates in lysosomes
- EM-level gives the lysosomes a "whirling" pattern
