Blake_Biochem_17_Membranes II Flashcards

1
Q

How is membrane fluidity controlled?

A

Fatty acid composition

Cholesterol content

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2
Q

How does fatty acid composition control membrane fluidity?

A
  • Length of the fatty acid chain
  • Saturation levels (Tm, rigidity)
  • Position of double bonds
    • cis-position produces bends
    • effects Tm, provides more fluidity
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3
Q

How is lateral movement of membrane proteins proven?

A

FRAP - fluorescence recovery after photo-bleaching

Rate of recovery of fluorescense depends on the lateral mobility of the fluorescent labled component

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4
Q

How is lateral movement of phospholipids in a membrane different from transverse diffusion?

A

Lateral movement is very rapid, transverse is very slow

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5
Q

What is significant about the asymetrical distribution of lipid molecules?

A

Explains many phenomena

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6
Q

Why are carbohydrates placed on the cell membrane?

Types of membrane carbs

specific membrane carbs

functions of membrane carbs

A
  • carbohydrates, glycoproteins, glycolipids
  • Glycosylation occurs on extracellular surface of the plasma membrane
  • Glycocalyx participates in cell adhesion, lymphocyte homing….
  • Contributes to cell identification
  • Antibodies target foreign carbohydrate molecules
    • antibodies recognize red blood cells’ blood types by extracellular carbohydrates
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7
Q

How are Eukaryotic cells distinguished from prokaryotic cells?

A
  • membranous internal compartments:
    • peroxisomes
    • mitochondria
    • endoplasmic reticulum
    • golgi apparatus
  • Eukaryotic cells have no cell walls
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8
Q

How are inner membranes of eukaryotic organelles different from outer membranes?

A

Inner membranes are not permeable

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9
Q

How is the nuclear envelope different from other eukaryotic organelles?

A

Nuclear envelope is not continuous; consists of closed membranes that come togehter in nuclear pores

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10
Q

Membranes must be able to: (3)

A
  • separate and join together so that:
    • take-up
    • transport
    • release the molecules
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11
Q

RME

A

Receptor-mediated endo/exocytosis

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12
Q

Receptor-mediated endocytosis: “Budding”

process

A

“Budding”

  • signal binds receptor
  • membrane invaginates around ligand bound receptor
  • Invaginated membrane breaks off and fuses to form a vesicle
  • signal and receptor are disociated
  • receptors are recycled
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13
Q

RME “Fusion”

A
  • eg: fusion of a vesicle to a membrane is key for neurotransmitter release into synaptic cleft
  • SNARE: gathers appropriate membranes to initiate fusion process (many intermediates)
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14
Q

Mitochondrial Fission

A
  • Mitochondria “pinches” and divides into 2 mitochondria
  • DRP1 oligomers facilitiate pinching and vessical scission
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15
Q

How many genes in Mitochondrial genome?

A

13

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16
Q

Where are most mitochondrial proteins encoded?

A

from Cellular DNA

17
Q

How does mitochondrial fusion occur?

A
  • Collision in movement of organelles along microtubules
  • dying mitochondria signal to healthy mitochondria so that fusion can salvage usable components
18
Q

Why does mitochondrial fission occur?

A

to prepair the cell for mitotic division

19
Q

Requirements for inner-membrane fusion:

A
  • Sufficiently large electrochemical gradient must be present across inner membrane
  • Elevated GTP levels must be available for hydrolysis
20
Q

Control of fusion/fission mechanisms in mitochondria

A

unknown

21
Q

Protein import into mitochondria (4)

A
  • N-terminal signal sequence - matrix targeting
  • proteins are unfolded and threaded through “import pores
  • Refolded inside the mitochondrial target
  • Transient channels (both outer and inner membranes) are necessary for intra-matrix proteins