Lecture 8 Flashcards

1
Q

RNA pol I makes which rRNA?

A

47S rRNA

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2
Q

RNA pol II makes what?

A

mRNA

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3
Q

RNA pol III makes what ?

A

5S rRNA, tRNA

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4
Q

mRNA transport

A

-Nucleus to cytoplasm
-Ran independent pathway
-Uses TAP

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5
Q

tRNA transport?

A

-Nucleus to cytoplasm
-Uses exporting-t needs Ran

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6
Q

rRNA transport

A

-Nucleus to cytoplasm
-Ran depended
Crm1 part of importin beta family

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7
Q

snRNA transport?

A

Nucleus to cytoplasm
Ran dependent

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8
Q

Signals needed for mRNA transport?

A
  1. 5’ cap
  2. Poly-A tail
  3. Absence of introns
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9
Q

Energy used to transport mRNA to cytoplasm?

A

-ATP

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10
Q

Transport factors needed for mRNA transport?

A

-RNA helicases
-Nucleoporins Nup98
-TAPs

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11
Q

Why does incompletely spliced mRNA HIV reside in the cytoplasm?

A

-mRNA comes from the virus
-Have Rev response element which is recognized by Rev when this binds the NES is recognized by Crm1 and it allows the incompletely spliced mRNA to get from nucleus into the cytoplasmW

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12
Q

What happens if we eliminate Crm1?

A

You will die since you ribosomes can no longer be transported from the nucleus to the cytoplasm

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13
Q

Stess Granules

A

LLPS compartments

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14
Q

What are stress granules composed of?

A

Mostly RNA bidning proteins and different types of RNA

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15
Q

What happens if cell stress is chronic?

A

Stress granules will transition to a more gel-like consistency which cannot be disassembled
Wosrt case: fibrils will be generated which are permanent and damaging to the cell

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16
Q

T/F:The formation of stress granules is stress dependent and transient (get rid of the stress then you get rid of the stress granules)

A

T

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17
Q

What generates stress granules?

A

-Oxidative stress (hypoxia, kidney will generate stress granules), also seen after heart attacks or strokes)
Temperature stress (most relevant to humans (fever))
Changes in pH
Changes in salt

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18
Q

Why make stress granules?

A

-Recruit pro aptotic factors (prevent cell death)
-Protect mRNAs from degradation during stress

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19
Q

Where do stress granules assemble

A

Cytoplasm

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20
Q

Why is importin alpha 1 in Stress granules?

A

Helps assemble full sized SGs
Without importin-alpha 1 cells make smaller SGs and the cells are more prone to death when you stress them

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21
Q

SGs in cancer?

A

Chemotherapy stresses the cnacer cells causing them to form SGs which is harmful because cell is now less likely to die

22
Q

SGs in neurodegeneration?

A

If the granules become perisitent this can facilitate neurodegeneration

23
Q

SGs and viral infections

A

Granules are often generated for many virus infections this can be bad because viruses such as HIV interfere with the proper formation of SGs this makes the cell more prone to cell death and leads to increased infectivity

24
Q

Nuclear transport receptors can prevent/reduce the formation of permanent aggregates in the cell

A

Transportin I binds proteins and prevents them from aggregating

25
Q

Peroxisome trafficking

A

One way can only go from cytosol into the perozisome

26
Q

Peroxisome

A

-A bag of enzymes which are approximately 0.2 to 1 micron in diameter
Have a single membrane and a single matrix
Important for many detoxification reactions
Important for the degradation of long chain fatty acids
Important for the generation of myelin

27
Q

All proteins in the matrix of the peroxisome must be imported from the cytoplasm

28
Q

T/F: folded proteins can be transported into the peroxisomal matrix

29
Q

What does prtoein import into peroxisomal matrix require(energy)?

30
Q

Peroxins

A

PEX genes mediate peroxisomal biogenesis and protein import

31
Q

What mediated protein import into the peroxisomal matrix?

A

Transient translocon

32
Q

Is there a permanent pore in the peroxisome transport like NPC?

A

No, just a translocon

33
Q

Translocon contains a lot of YG domains which fill the lumen of the translocon opening

A

Come from PEX13
PEX5 associates with the YG domains and the cargo and then it is translocated into the matrix

34
Q

PEX5 recycling

A

Reversible ubiquitination moves PEX5 back to cytoplasm

35
Q

Translocon pore is smaller than NPC?

A

Ture can only fit 2nm

36
Q

Mutation in PEX5

A

Zellweger syndrome
Causes proteins destined for the peroxisome to not be transported

37
Q

Mutation in PTS sequence

A

mistargeting of the protein to the mitochondria

38
Q

PEX5 recognizes

A

SKL(C-terminus sequence)

39
Q

PEX7 recognizes

A

PTS-2(N-terminus sequence)

40
Q

Compartments of mitochondria?

A

Outer mitochondrial membrane
Inner mitochondrial membrane
Intermembrane space
Matrix

41
Q

Actins are globular protein

42
Q

Treadmilling(actin)

A

Rate of adding and dissociating is the same. Monomers move through actin

43
Q

What causes monomers to dissociate from actin?

A

ATP hydrolysis

44
Q

Proffin

A

Binds actin and prevents nucleation event and filament formation

45
Q

Dynamic instability of microtubules?

A

Microtubules shoot out from an organizing center from plus end to minus end

46
Q

Beta-tubulin

A

Beta-tubulins bind to GTP and the GTP is hydrolyzed to conduct dynamic instability

47
Q

Rate constant of NTP form is larger

A

Both actin and microtubules like to polymerize when bound to NTPs

48
Q

When microtubules and actin are bound to GDP?

A

Filaments like to diassemble

49
Q

ATP/GTP caps

A

Form when we add more ATP or GTP to the filament then we are dissociating

50
Q

Loss of ATP/GTP caps

A

Hydrolysis becomes faster than addition of NTP and microtubules/actin quickly diassemble

51
Q

Monomers can add to both the plus and minus side