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Cell & Tissue Biology > Exam #1: Cell Biology IV > Flashcards

Exam #1: Cell Biology IV Flashcards

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1
Q

How are phospholipids synthesized?

A
  • Phospholipids are synthesized on the cytosolic monolayer

- Scramblase flips the phospholipids into the other monolayer, maintaining symmetry

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2
Q

Scramblase

A
  • Flips phospholipids from on monolayer into another

- Maintains membrane monolayer symmetry

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3
Q

What happens when additional plasma membrane is no longer needed?

A

Macroautophagy

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4
Q

Phospholipid Exchange Protein

A

transfers phospholipids from the ER to another membrane in the cell

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5
Q

What is Atlastin?

A
  • GTPase that is involved in constructing & shaping the ER

- ER scaffold protein

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6
Q

Atlastin Abundance

A

Increased ER membrane fusion & absence of Golgi

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7
Q

Atlastin Deficiency

A
  • ER becomes fragmented

- Hereditary Spastic Paraplegia

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8
Q

Hereditary Spastic Paraplegia

A
  • Caused by Atlastin deficiency

- Leg stiffness, gait disturbances, facial dysmorphia

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9
Q

Proteasome

A
  • In BOTH cytosol & nucleus
  • MOST are ubiquitin dependent, but NOT all
  • Energy dependent
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10
Q

What are examples of things that are eliminated by proteasomes?

A
  • Cyclin/CDKs (mitotic factors)

- CFTR

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11
Q

What disease states inhibit proteasome action?

A
  • Prion proteins (Creutzfled Jacob Disease)
  • Amyloid (Alzheimer’s Disease)
  • Lewy Bodies (PD)
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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
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13
Q

Golgi Apparatus

A
  • Situated near the nucleus

- Contains cisternae (sacs)

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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
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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
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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
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17
Q

Ceruloplasmin

A
  • Major copper-binding protein in the blood

- Binds copper in the Golgi apparatus & then excreted into the blood

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18
Q

Apoceruloplasmin

A

Copper not bound to binding protein

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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
Q

Trans Golgi Network

A

Secretes vesicles

26
Q

Endosomal Compartments

A
  • Near the cell membrane
  • Early & recycling endosome
  • Multivesicular Body
  • Late endosome
27
Q

Lysosomal Compartments

A
  • Close to the interior of the cell

-

28
Q

Early Endosome

A
  • Located in the cell’s periphery

- pH 6.2-6.5

29
Q

Recycling Endosome

A
  • Just beneath the plasma membrane
  • Store membrane proteins e.g. glucose transporters
  • Insulin binding, insert glucose transporters into the plasma membrane
30
Q

Multivesicular Body

A
  • Deeper than early endosome
  • Budd off the early endosome
  • Transported along microtubules to late endosome
  • pH 5.0- 6.2
  • Origin of exosomes
31
Q

Late Endosome

A
  • Fuse with multivesicular bodies
  • pH ~5.0
  • Fuse with or mature into lysosomes
32
Q

What controls the acidity of the endosomal and lysosomal compartments?

A

H+-ATPase

33
Q

Fates of Endocytosed Receptors & Ligands

A
  • 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
Q

What uncouples receptors & ligands when the receptor is recycled and the ligand is not?

A

Acidic pH of the early endosome

35
Q

Achondroplasia

A
  • 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
Q

Transport of Lysosomal Hydrolases

A
  • Lysosomal Hydrolase Precursor is tagged with mannose
  • Cis–>Trans Golgi
  • Mannose 6-phosphate receptor recognizes the mannose tag
  • Delivered to endosome or lysosome
37
Q

At what pH are lysosomal hydrolases most effective?

A

Low

38
Q

What are the different pathways used to degrade material?

A
  • Autophagic
39
Q

What are the different autophagic processes?

A

1) Macroautophagy (organelles)

2) Microautophagy (protein)/ Chaperone-mediated autophagy

40
Q

Heterophagosome

A
  • Contains something that was brought in from the external environment to be degraded
  • vs. autophagosome
41
Q

Heterophagolysosome

A
  • Heterophagosome fused with lysosome

- Secondary lysosome

42
Q

Residual Body

A
  • Material that could not be digested by the lysosome

- Forms lipofuscin

43
Q

What is special about osteoclasts?

A

Secrete lysosomal hydrolyses for degradation of bone material

44
Q

Primary Lysosome

A
  • Not degrading anything/ has not received a phagosome

- Homogenous

45
Q

Secondary Lysosome

A
  • Fused with phagosome
  • Degrading material
  • Heterogenous (light & dark)
46
Q

Pompe Disease

A
  • Caused by a defect in the delivery of the lysosomal hydrolases to the lysosome
  • Glycogen storage disorder, where glycogen accumulates in lysosomes
47
Q

Tay-Sachs Disease

A
  • Deficiency in the enzyme that breaks down sphingolipids
  • Lipid material accumulates in lysosomes
  • EM-level gives the lysosomes a “whirling” pattern

Cell & Tissue Biology (25 decks)

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