Membraan biogenese 3 Flashcards

1
Q

Explain the process of transporting lipids from the ER to mitochondria, focusing on the conversion of PS to PE in mitochondria.

A

Lipid transport from the ER to mitochondria involves the conversion of PS to PE in mitochondria, with enzymes located in both organelles. This process is crucial for glycerophospholipid synthesis.

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2
Q

Why is bulk transport necessary for the conversion of PS to PE in mitochondria? Provide an example.

A

Bulk transport is necessary because, for instance, PA (used for CL synthesis) is made in the ER but needs to be transported to mitochondria. Bulk transport ensures the efficient movement of lipids between these organelles.

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3
Q

Describe the different mechanisms of lipid transport between membranes. Why is spontaneous diffusion inefficient for hydrophobic fatty acid tails?

A

Mechanisms include spontaneous diffusion, protein-mediated transport, vesicle flux, and membrane contact/fusion. Spontaneous diffusion is inefficient due to the reluctance of hydrophobic fatty acid tails to leave the membrane.

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4
Q

How do integral membrane proteins play a role in the balance of lipid membrane growth in the ER?

A

Lipid membrane growth in the ER is balanced by flippase proteins, which redistribute lipids by flipping hydrophilic heads across the membrane. This prevents instability in the membrane.

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5
Q

What is the flip-flop model for phospholipid transport in biogenic membranes?

A

The flip-flop model suggests that the dynamic behavior of hydrophobic membrane-spanning proteins causes transient defects in the lipid-helix interface, allowing phospholipids to flip over the bilayer.

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6
Q

Explain the asymmetrical lipid distribution in the plasma membrane. How is this maintained?

A

Amino phospholipids like PS and PE are predominantly on the cytoplasmic side, while PC is enriched on the outer side. Asymmetry is maintained by processes in the Golgi, involving synthesis and transporters.

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7
Q

How is the regulation of cholesterol biosynthesis achieved in response to ER cholesterol levels?

A

The SREBP-2 sensor-effector system regulates cholesterol synthesis. SREBP is a transcription factor that responds to low ER cholesterol. When cholesterol is low, SREBP is transported to the Golgi, leading to increased transcription of HMG-CoA reductase.

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8
Q

Why is cholesterol important for membrane fluidity, and how is its synthesis regulated by statins?

A

Cholesterol regulates membrane fluidity. Statins, competitive inhibitors of HMG-CoA reductase, are used to reduce cholesterol synthesis, making them a therapeutic option for cardiovascular diseases.

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9
Q

What is the primary role of PS in the context of lipid transport from the ER to mitochondria?

a) PS acts as a signaling molecule.
b) PS is converted to PE in mitochondria.
c) PS is transported back to the ER.
d) PS forms a stable structure in the mitochondria.

A

B

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10
Q

What is the significance of bulk transport between the ER and mitochondria in lipid synthesis?

a) It reduces lipid synthesis efficiency.
b) It prevents lipid transport.
c) It ensures efficient movement of lipids between organelles.
d) It is irrelevant to lipid synthesis.

A

C

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11
Q

How do flippase proteins contribute to the stability of membranes in the ER?

a) They inhibit lipid synthesis.
b) They cause membrane instability.
c) They redistribute lipids, preventing membrane instability.
d) They are not involved in membrane stability.

A

C

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12
Q

According to the slip-pop model, what causes transient defects in the lipid-helix interface?

a) Spontaneous diffusion.
b) Membrane contact.
c) Hydrophobic membrane-spanning proteins.
d) Hydrophilic heads.

A

D

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13
Q

What contributes to the asymmetrical lipid distribution in the plasma membrane?

a) Random lipid movement.
b) Golgi synthesis of sphingolipids.
c) Bulk transport from the ER.
d) Flippase activity

A

B

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14
Q

How does the cell regulate cholesterol synthesis in response to low ER cholesterol levels?

a) By increasing HMG-CoA reductase transcription.
b) By decreasing SCAP binding to Insig.
c) By reducing SREBP transport to the Golgi.
d) By inhibiting P4-ATPase activity.

A

C

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15
Q

True/False: Lipid transport between ER and mitochondria involves vesicle flux.

A

F

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16
Q

T/F: The flip-flop model suggests that specific flippase proteins catalyze lipid translocation in membranes.

A

F

17
Q

T/F: Cholesterol synthesis is regulated by the SREBP-2 sensor-effector system, where SREBP is transported to the Golgi in response to high ER cholesterol.

A

F

18
Q

Spontaneous diffusion

A

Hydrophilic and hydrophobic regions of lipids cause movement in the membrane.

19
Q

Vesicle flux

A

Common in secretory routes, not efficient for ER-mitochondria lipid transport.

20
Q

Membrane contact/fusion

A

Lipids may cross membranes through contact or fusion, challenging due to different lipid compositions in ER and mitochondria.

21
Q

Bulk transport is necessary for the conversion of __________ to __________ in mitochondria.

A

PS to PE

22
Q

The slip-pop model suggests that the dynamic behavior of __________ proteins causes transient defects in the lipid-helix interface.

A

Hydrophobic membrane-spanning

23
Q

Explain the role of the ERMES complex in lipid transport between the ER and mitochondria.

A

The ERMES complex forms a tunnel-like structure that facilitates the bulk transport of lipids between ER and mitochondrial membranes.

24
Q

What is the significance of the 5% cholesterol threshold in the ER for the regulation of cholesterol synthesis?

A

Below 5% cholesterol, the SREBP-2 system is triggered, leading to increased transcription of HMG-CoA reductase, promoting cholesterol synthesis.

25
Q

Interpret the figure showing the ER-mitochondria contact in a hepatocyte. What does the close apposition of ER and the outer mitochondrial membrane suggest?

A

The close apposition suggests membrane contact and/or temporary fusion, indicating the importance of these interactions in lipid bulk transport.