Lecture 4 Flashcards

(33 cards)

1
Q

How many RNA polymerases exist in eukaryotes?

A
  1. RNA Poly I/ II and III
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2
Q

What is an active enzyme complex called?

A

Holoenzyme

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3
Q

What is the function of RNA Poly I and III?

A

Ribosomal and tRNA synthesis

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4
Q

What is the function of RNA Poly II?

A

Protein coding genes

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5
Q

What are they key steps of the Transcriptional Process?

A

Initiation: Recruits Polymerase
Pause Release
Elongation

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6
Q

What is the assembly of Polymerase called?

A

Pre-Initiation complex

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7
Q

What is a Transcription Factor?

A

Protein involved in transcriptional initiation or elongation or in their regulation

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8
Q

What is a promoter?

A

Regulatory DNA sequence. Defines transcription start site

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9
Q

What is the TATA box?

A

AT-rich sequence: Recruites TATA binding protein (TBP) and (TBP associated factor) TAF

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10
Q

What do TAFs do?

A

Mediate contacts to other transcription factors

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11
Q

What is the assembly of the pre-initiation complex?

A

Promoter recognition: TFIID recognizes promoter and binds via (TATA binding protein) TBP
Assembly of Transcription factors:
RNA PolyII is recruited to promoter region.
TFIIH helps unwind the DNA
Formation of Pre-initiation complex by all transcription factors and RNA Poly II
Initiation: TFIIH phosphorylates C-terminal RNA Poly II and initiates transcription elongation

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12
Q

How many bp are transcribed after the first transcription elongation? And why is that?

A

Only about 20-30. Pause-release -> second phophorylation at CTD occurs. This is done to keep genes “ready to be transcribed” -> transcription can occure faster if genes are already prepared

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13
Q

When does splicing occure?

A

Co-transcriptionally

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14
Q

What is the poly-A signal used for?

A

Transcription termination

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15
Q

What is ATP used for in Transcription?

A

As hydrolysis target in transcription initiation

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16
Q

What is the negative control of transcription regulation at the promoter level?

A

Activation by absence of repressor, but repressor needs to be constantly present

17
Q

What is the positive control of transcription regulation at the promoter level?

A

Activation by presence of activator, activator only neden when transcription occurs

18
Q

What are promoter functions and where do they lie?

A

Next to transcription start site and they are needed for RNA pol II positioning, and can bind repressors (regulation)

19
Q

What does gene control of transcription factors depend on?

A

Availability of factor
Accesibility of DNA
Activity of factor

20
Q

What are common features of transcription factors?

A

DNA-binding
binds DNA as dimers
co-operate with other factors
mediate transcription activation

21
Q

How does the glucocorticoid receptor work?

A

Steroid replaces nucleosome and opens a binding site for Transcription factor to activate transcription (normally blocked by nucleosome)

22
Q

What is a co-activator?

A

Does not bind DNA itself but mediates transcription by interacting with Transcription factors

23
Q

What is the most ubiquitous co-activator of transcription

A

Mediator Complex

24
Q

What does the mediator complex do?

A

Mediator complex receives signals from Transcription factors and transcmits them to RNA poly II

25
Can Transcription be fine tuned?
Yes by several factors working in tandem.
26
What are enhancers?
Regulate transcription far away from promoter
27
How do enhancers act?
Regulate through proximity in space
28
How do enhancers work?
Chromatine remodleing or direct interaction with transcription machinery
29
What is a multi-TF complex on enhancercalled?
Enhancosome
30
What is a super enhancer?
Multiple enhancers acting together high density of TF binding sites increased transcriptional activation sustained transcriptional activation
31
Transcription in 5 steps
1: Transcription factor recruitment and remodeling of Nucleosomes 2:Pol II recruitment and progression to start site 3: signal-pause release, beginning of Transcription
32
What are transcription factories?
local concentrations of Transcription factors, RNA Poly and co-activators etc in the nucelus
33
How does MYC become hyperactive in cancer?
By interchromosomal translocation of enhancers -> leads to enhancer duplication -> increase in transcription