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Enzymes > Transcription, RNA processing and control of Gene expression > Flashcards

Transcription, RNA processing and control of Gene expression Flashcards

1
Q

What are the four rRNA molecules, and where do each of them come from?

A

There is 28S, 18S, 5.8S and 5S. All except for 5S come from Pol I, 5S is made by Pol III

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2
Q

What does Pol III synthesize?

A

The 5S rRNA, as well as tRNAs.

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3
Q

True or false: G, U, A, C, and inosine are common to tRNAs

A

True

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4
Q

What does pol II synthesize?

A

mRNA

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5
Q

What is the function of the TATA boxes, CAAT box, and GC region?

A

Generally a promoter region for Pol II (TATA especially)

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6
Q

How do the promotor regions help Pol II begin synthesis?

A

bind proteins which help Pol II bind

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7
Q

True or false: Pol II can bind to promotor regions without the help of general transcription factors

A

False (for our purposes at least)

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8
Q

What is TFDII?

A

A complex of binding proteins that help RNA Pol II bind

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9
Q

TBP is what?

A

The TATA binding protein, part of TFDII, the specifically binds to the TATA box and acts as a signpost for other proteins to bind

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10
Q

What are the other transcription complexes besides TFIID?

A

TFIIE, TFIIF, and TFIIH

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11
Q

Which pairs are easier to pull apart, A-T or G-C?

A

A-T

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12
Q

Which general transcription factor has DNA helicase activity?

A

TFIIH

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13
Q

True or false: the transcription factors stay attached to RNA Pol II once transcription begins

A

False

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14
Q

What is the basal transcription complex?

A

The complex of RNA and general transcription factors that help pol II bind

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15
Q

What does SP-1 bind to? What does it do?

A

GC-rich sequences

Increases Pol activity above the basal rate

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16
Q

What does NF1 bind to? What does it do?

A

CAAT boxes

Increases Pol activity above the basal rate

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17
Q

What is required for transcription of tightly bound chromatin?

A

Chromatin remodeling

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18
Q

What is the primary mechanism for Death Cap Mushroom?

A

Inhibition of Pol II, blocking the synthesis of mRNA

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19
Q

What is the mechanism by which the abx Rifampicin works? What notable disease is the used as treatment for?

A

Inhibits the prokaryotic RNA polymerase II

TB

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20
Q

What does pre-mRNA contain? How are these removed?

A

Exons and introns

By splicing

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21
Q

What are the enzymes that catalyze RNA splicing?

A

Spliceosomes

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22
Q

What are the three important sites involved in RNA splicing?

A

5’ splice site
3’ splice site
a branch point

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23
Q

What is the base that is at the branch point in RNA splicing? What does it attack (5’ or 3’ splice site)?

A

Adenine

Attacks the 5’ splice site

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24
Q

How does tropomyosin have a wide variety of isozymes (hint: think about exons)

A

Different branch points produce different exons

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25
Q

What molecules is used in the 5’ cap?

A

Methylguanasine

26
Q

What is the polyadenylation signal?

A

The DNA encoded part of the RNA that specifies where the poly A tail should be placed

27
Q

What does the Poly A tail consist of?

A

around 200 Adednine nucleotides

28
Q

Export of mRNAs out of the nucleus is highyl regulated–what do mRNAs NEED to have, in order to leave the nucleus?

A

Poly A tail, and 5’ cap

29
Q

Which is degrated first: the 5’ cap or the poly A tail?

A

Tail first, then cap

30
Q

What are the enzymes that degrade the mRNA molecule?

A

Ribonucleases

31
Q

What is beta-thalassemia? What is it caused by?

A

It is the reduced synthesis of the b-globin chain of Hb, leading to profound anemia.

This is caused by a gene mutation that alters the base at the boundary of the first exon, leading to incorrect splicing. The correct protein is NEVER produced.

32
Q

PKU is the result of defective phenylalanin hydroxylase. How is this defect brought about?

A

There is a single change in the 5’ splice dnor site culminating in a truncated mRNA and thus non-functioning protein

33
Q

What are chromatin remodeling complexes?

A

large, multisubunit complexes that use ATP to change structure of nucleosomes temporarily so that DNA is less tightly bound to the histone.

34
Q

What do histone acetyltransferases (HATs) do?

A

acetylate various particular K residues in the histones, reducing the positive charge of the histone, and thereby reducing the association with DNA

35
Q

What do histone deacetylases (HDACs) do?

A

Opposite of HATs

36
Q

What sort of chemical change to histones would you expect very active regions of DNA transcription to have?

A

Hyperacetylation

37
Q

What does the methylation of cytosine do?

A

Inhibits transcription of the DNA it is associated with, by binding transcription silencing proteins.

(no effect on base pairing)

38
Q

Where do DNA binding proteins bind to?

A

To exposed portion of bases in the major groove of the helix

39
Q

What are the three types of gene regulartory proteins?

A

Helix-turn-helix
Zinc finger
Leucine zipper

40
Q

The helix-turn-helix proteins consist of a helix, small polypeptide chain, and another helix. What part of the protein is involved in binding to the DNA?

A

The amino acids in the more C-terminal side of the protein

41
Q

What is the structure of Leucine zippers like?

A

Two alpha helicies join together to form a coiled-coil.

Each helix has a hydrophobic residue (usually K) at every 7th position

42
Q

What, generally, is the action of the leucine zipper, zinc finger, and helix-turn-helix proteins?

A

Bind to DNA and recruit HATs (or HDACs)

43
Q

The promoter region of the LDL-receptor gene contain what particular region of DNA? What does it do?

A

SRE-1 (sterol responsive element-1)

Promotes cholesterol affiliated gene synthesis

44
Q

What is CRSP?

A

A protein that helps SP-1 bind to the GC boxes, and aid in the transcription of LDL receptor gene

45
Q

What is SREBP-1a? What does it do?

A

The sterol responsive binding protein 1a.

It is maintained outside the nucleus unless cholesterol levels falls–then goes in to bind to SRE-1 and recruit a HAT–increases transcription

46
Q

What is rubinstein_taybi syndrome?

A

A disease characterized by MR, and other abnormalities, due to the genes encoding EP300 or CBP

47
Q

PKA is able to gain transcriptional control of PEP carboxykinase via what mechanism? (describe it, there are 3 additional proteins utilized)

A

PKA phosphorylates CREB which then binds To CRE, which recruits EP300.

CRE/EP300 act as HATs for the PEP carboxykinase gene

48
Q

What is tamoxifen, and how does it exert its effects?

A

Inhibits cancer growth by competitivly inhibiting the DNA-binding receptor proteins.

49
Q

Where is the thyroid hormone receptor usually found?

A

Bound to the DNA–it represses transcription

50
Q

What is the protein that the thyroid hormone receptor bound to

A

RXR, which binds an HDAC

51
Q

What happens when the thyroid hormone binds to thyroid hormone?

A

THR undergoes a conformational change, and binds a HAT

52
Q

Which enzymes does PKA increase the transcriotion of?

A

Hormone Sensitive Lipase and PEPCK

53
Q

What is the DNA binding site that is involved in the PKA pathway to increase transcription?

A

CRE

54
Q

PKA phosphorylates what protein to attach to CRE?

A

CREB

55
Q

What is the protein that attaches to a phophorylated CREB protein sitting on a CRE?

A

CBP and EP300

56
Q

What is the function of CBP/EP300 complex?

A

Recruit a HAT protein to the CRE site and allow fro transcription of PEPCK

57
Q

What is Rubinstein-Taybi syndrome?

A

MR due to mutations in the CBP or EP300 proteins.

58
Q

Where is the cortisol receptor found?

A

The cytoplasm

59
Q

What prevents the cortisol receptor from entering the nucleus and activating transcription?

A

It is masked until cortisol binds to it.

Then conformational change

60
Q

What is the promoter element for cortisol called?

A

GRE (glucocorticoid responsive element)

61
Q

The LCL receptor gene recognizes what protein signals on the outside of VLDLs/LDLs?

A

Apoprotein E and B

62
Q

Basal transcription of the LDL receptor gene involves what promoter region, with what protein?

A

GC rich region with SP-1/CRSP binding to it.

Enzymes (24 decks)

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