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MSI Unit I > 1-44 Eukaryotic Transcription I > Flashcards

1-44 Eukaryotic Transcription I Flashcards

1
Q

RNA polymerase 3 types and what they do

A

three types exist in eukaryotes
1. pol 1 (transcription of most ribosomal RNA’s)

  1. pol II (mRNA’s, mi, Inc,sn and snoRNA’s)
  2. pol 3 (tRNA’s, 5s r RNA ribososomal precursor, snoRNA’s, and other small RNAs)
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2
Q

why does Pol II pause?

A

regulatory step - Pol II is paused shortly after trancription begins.

pol II must be released from pause site in order for elongation to proceed

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3
Q

what do transcription factors do?

A

bind to enhancer sequences that can be far from the gene being transcribed. act by recruiting a mediator protein or chromatin modifier

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4
Q

what are enhancer sequences composed of?

A

DNA binding domain and an activation or repression domain (depending on if it up or down regulates transcription)

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5
Q

What do the parts of the enhancer sequences d?

A

DNA binding domain - provides specificity to its particular enhancer sequence

Activation/repression domain provides its up or down regulatory function

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6
Q

the DNA binding domain and activation/repression domains are both..

A

modular - meaning the binding domain can be combined with the activation/repression domain of another

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7
Q

if one domain is mutation

implications in cancer evolution?

example?

A

the other domain can function normally

-implications in cancer evolution. Mutations in either site can affect the action of the transcription factor to the point of causing disease

(actute lymphoblastic leukemia)

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8
Q

what are transcription mediators?

A

complex of proteins that bridges activatiors to RNA poly II and basal factors

required for transcription to begin

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9
Q

mediators are required for…

A

transcription to begin

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10
Q

chromatin modifiers are promising..

A

anticancer drugs

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11
Q

5’ capping

A

A 7-methylguanosine nucleotide is added to the 5’ end of the pre-mRNA. Helps to protect the mRNA from degradation, facilitate nuclear export, and allow translation by the ribosome.

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12
Q

3’-Polyadenylation

A

– Over one-hundred adenine nucleotides are added to the 3’ end of the pre-mRNA, past the poly (A) addition signal. Provides the benefits as the 5’-cap.

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13
Q

Splicing

A

pre-mRNA have introns spliced out leaving exons.

alternative splicing allows for more than 1 distinct protein to be transcribed from a single DNA sequecne

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14
Q

the end result of hormones?

A

hormones stimulate signal trasduction pathways leading to trasncription activation or repression

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15
Q

Rna polymerase uses what type of precursors?

A

ribonucleodies, not deoxyribonucleotides

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16
Q

RNA polymerases share many

A

basal factors

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17
Q

general initiation steps

A
  1. TBP portion of TFIID binds TATA box to bend DNA
  2. TBP and other general basal TF help recruit RNA poly 2 to promoter (forms pre-initiation complex)
  3. Pol II must be phosphorylated to leave promotor and start transcribing mRNA
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18
Q

antibiotic against trasncription?

A

Vancomycin. binds to DNA and blocks ability of Pol I and Pol II to elongate

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19
Q

Eurkaryotic RNA polymerases need basal TF factors to…

A

recognize promotor and form initiation ccomplex

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20
Q

what are enhancers and what do they do?

A

cis acting sequences located far away from gene in loops where TF interacts with complex called mediator.

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21
Q

Eukaryotic trasncription factors do what to stimulate RNA pol II?

A

bind enhancers

22
Q

t-cell acute lymphocytic luekemia

A

caused by translocation of t-cell enhancer next to homeobox gene. This enahncer is evolved to be strong in T cells. So what happens is that now in t-cell you are making tons of hox11 protein. Way more than needed.

23
Q

what determines the specificity of transcription factors?

A

TF’s fold up well and typically have alpha helix that inserts into DNA major groove. Side chains touch bases in base pairs, determins specificity in what genes they target.

big alpha helix in base groove touches base pairs, multiple contacts gives specificity

works without having to unwind DNA helix.

24
Q

DNA site recognition is determined by?

A

amino acid-base pair interactions

25
Q

___________ is a trancriptional event.

defects in this cause?

A

differentiation

defects in transcription can block differentiation and contribute to cancer development. Cells stay in immature state and continue to divdie

26
Q

what is p53

A

is a tumor suppressor transcription factor that binds DNA and can repress or activate

27
Q

mutations in TF are

A

oncogenic

28
Q

how do TF factors control rates of trasncription?

A

stimulate/repress general transciption machinery

recruit crhomatin modifiers or negative chromatin modifiers (to repress)

29
Q

chromatin modifiers target _________

major types?

A

histone N-terminal tails

acetylation (Activation)
de-acetylation (repression)
methylation (activation or repression)

phosphorylation (coupled to acetylation)

30
Q

it is beleived that the histone N-terminal tail modifications serve as…

A

binding sites for enzymes involved in trasncription

31
Q

3 types of epigenetic modifiers

A

writers - place modification on n-terminal tail or methylate DNA

erasers - remove modifications

Readers -enzymes for transcription

32
Q

drugs to inhibit or stimulate modification enzymes

A

want to decrease cancer

  1. block ability of histone acetyltransferase (HAT) to put acetyl group on histone, activating it. Add HAT to an ocogne, you can repress it.
  2. 5-aza-cytodine - traps enzyme that maintains chemical modifications after replication. methlation is lost after successive replication cycles. CpG becomes under-methylated, and turns ON tumor suppressor genes.
  3. Target erasers - chromosome stays acetylated (activated) by blocking de-acetylases (HDAC inhibitors) which deactivate the gnene by removing teh acetyl grou;.
33
Q

Bet inhibitor is what type of promising drug approach?

A

drugs that target chromatin readers
-BET inhibitor prevents bromodomain in readers from binding to acetylated histones (otherwise active histones). Block the reader from reading/binding.

Block Bet domain, can no longer bind and express the onco gene.

34
Q

why does POL II pause?

A

negative elongation factors conact polymerase and recognize pause sites

the P-TefB kinase phosphorylates the negative elongation factors to fall off or become position elogation factors.

35
Q

Myc oncoprotein does what?

A

binds enahncer DNA and helps recruit positive elongation factors (P-TEFb) resulting in upregulation of many genes by increased transition to elongation

36
Q

3 types of burketts lymphoma

all associated with?

A

sporatic, endemic, immunodeficicny related

translocation in which immunglobulin enhancer gets juxtaposed next to oncogene promoter.

translocation leads to way too much elongation factor c-Myc. Myc is a factor for many genes trhoughout the gene so it is hard to target
-get elongation at many genes, lots of genes mis expressed

37
Q

how can we nullify the effects of excess Myc?

A

Myc acts on many genes, it would be impossible to target them all. Better to use bet inhibitor to shut off Myc itself

38
Q

TF help recruit

A

RNA pol 2 OR enzymes that modify chromatin structure and chemistry

39
Q

what do chromatin modifiers do?

A

add covalent modifications to histone n-terminal tails

40
Q

what types of modifcations do chromatin modifiers do?

A

activate via acetylation
deacetylate to deactivate
methylate to activate or repress (usually repress)

or phosphorylate, which is coupled to acetylation

41
Q

what recruits chromatin modifiers?

A

transcription factors

42
Q

2 classes of chromatin modifiers

A

histone modifying enzymes and

chromatin remodeling complexes that remodel nucleosomes

43
Q

histone tails are modified heavily and can lead to..

A

protein code regulation with readers, writers, and erases

44
Q

writer

A

place modification on n-terminal tail (acetylation or methylation)

OR methylate DNA

45
Q

erasers

A

remove modifications (deacetylate)

46
Q

readers

A

enzymes that read and act upon these modifications

47
Q

three things about modifications

A

they can occur in DNA or histones

they can be reversed

they can be inherited

48
Q

fight cancer using histone drugs (4)

A
  1. Block Oncogene - use HAT inhibitor to block HAT from acetylating the histone (activating the gene). block oncogene
  2. Upregulate tumor suppressor genes - Use drug like 5-aza-cytodine to trap DNA-methyl transferase that maintains modification of new strand after replication. Can decrease methylation on tumor suppessor gene to upregulate suppression ability
  3. Block erasers to prevent deacetylation (deactivation)- target the eraser (HDAC Histone Deacetylase complex) with HDAC inhibitor. tumor Repressor Gene stays acetalyated (active)
  4. Block the reader from binding - BET Inhibitor prevents the bromodomain from binding to acetylated (Activated) histones. may work by downregulating c-MYC
49
Q

oncogones and viruses mess with transcription at the level of

A

elongation

50
Q

what does the Myc oncoprotein do?

A

after the negative elongation factors bind and cause RNA pol II to pause, Myc binds to enhancer and recruits positive eleongation factor (P-TEFb)

51
Q

what does the activity of Myc do?

A

regults in upregulation of many genes via increaed transition to elongation

52
Q

what do the three types of burketts lymphoma all have in common?

treatment?

A

all caused by translocation of immunoglobulin enhancer to the oncogene promoter.

  • get lots of genes that are all misexpressed
  • caused primarily by Myc

instead of targeting all the genes, target Myc with BET inhibitors

MSI Unit I (52 decks)

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