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Block 1 Week 1 > Gene Expression > Flashcards

Gene Expression Flashcards

1
Q

How many base pairs in the human genome? How many genes does that encode?

A

-3 billion base pairs encodes 20,000-25,000 genes

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2
Q

What does RNA Polymerase 2 transcribe?

A

-transcribes DNA–> RNA, which then goes to encode proteins and miRNA

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3
Q

How are genes expressed (3 ways)?

A

1) constitutively (always) or induced (turned on at specific moments)
2) Ubiquitously (everywhere) or only in specific tissues/cell types
3) developmentally (prenatally) or temporally expressed (at a specific age)

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4
Q

Wha happens if the central dogma is interrupted?

A

If central dogma interrupted in transcription, RNA processing, or translation, it often leads to disease
-called dysregulation

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5
Q

What is involved in regulating gene expression?

A

1) proteins (transcritpion factors, co-regulators)

2) RNA (miRNA)

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6
Q

Typical structure of eukaryotic mRNA before processing (primary transcript)?

A
  • mRNA is modular, it requires distinct steps to reach final mature state
  • before processing, mRNA has:
    1) Exons
    2) Introns
    3) goes 5’–>3’
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7
Q

Structure of mature mRNA?

A

1) deletion of introns
2) 5’ cap
3) 3’ poly A tail

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8
Q

Where are exons in the mRNA mature transcript?

A

Exons can be

1) in the coding/translated region to be translated into proteins
2) can be in either the 5’ or 3’ untranslated region and in involved in regulation in trx or trans.

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9
Q

ORF mean?

A

open reading frame, the section that gets translated into protein

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10
Q

Differential mRNA splicing lead to?

A

A transcriptome that is much greater than the number of genes in our genome
-each gene can be transcribed into mRNA then processed in many different ways leading to many possibilities for the single mature mRNA we produce for a particular gene

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11
Q

transcriptome?

A

the sum total of all potential mRNA that can come from a gene

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12
Q

How does body decide which version of the mature mRNA it should make? Or which splicing process?

A

Based on:

1) tissue specificity
2) development stage specificity
3) environment-specific mechanisms
- depends on what body/cells need & where are located

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13
Q

Describe the average human gene.

A

1) covers ~27kb
2) 7-9 exons
3) has 1-100+ splice variants
4) average coding sequence ~1500bp
5) avg protein ~50kD
* is AVERAGE, most are not like this & have great variability

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14
Q

What body system has the greatest splicing variants?

A

1) nervous system

2) immune system

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15
Q

What is the core promoter?

A

The minimum DNA sequence required for transcription initation

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16
Q

What are enhancers?

A

DNA elements that stimulate transcription from a distance

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17
Q

What are silencers? Where located?

A

1)DNA elements that repress transcription from a distance by binding transcription factors that repress gene expression
(also called REPRESSORS)
2) 100-1000s basepairs away, up or downstream of core promoter
3) not orientation dependent, so sequence can be forward or backward & still bind the TF repressor

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18
Q

What are transcription factors?

A

Proteins that help RNA polymerase 2 bind to the core promoter & participate in initiating transcription at specific times within specific cell types

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19
Q

Why are enhancers & repressors not orientation dependent?

A

Because of nature of dsDNA

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20
Q

What does the ideal promoter for transcription contain?

A
  • contains core DNA elements for trxn regulation
    1) TFIIB recognition element (BRE)
    2) TATA box
    3) INR initiator
    4) Downstream core promoter element (DPE)
  • most genes do NOT have all components
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21
Q

Downstream vs upstream on the DNA

A 
Downstream= 3' end 
Upstream= 5' end
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22
Q

Where is the TATA box and TFIIB recognition element located?

A

Upstream of the initiator, this implies that they are in the 5’ untranslated region of the gene

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23
Q

How is specific DNA sequences transcribed in RNA in our individual cells?

A
  • each cell has the entire genetic info of organism
  • selective expression of the genome is tissue & organ dependent
  • each cell type expresses a unique set of genes which carry out the cellular functions
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24
Q

what are transcription factors?

A
  • Trxn factors are proteins that regulate gene expression
  • bind specific DNA sequences in the promoter of genes to affect trxn activity
  • multiple can work together to direct gene expression
25
Q

What are co-factors?

A

a non-protein, chemical or metallic ion that helps trxn factors regulate gene expression in specific cells

26
Q

What/where do trxn factors usually bind?

A

Bind to enhancer/repressor sequences upstream of the promoter or the promoter sequence itself
-activate or inhibit gene expression

27
Q

Where are/what are enhancers?

A
  • DNA sequences that increase gene expression
  • 100-1000s bp long
  • up or downstream
  • not orientation dependent (due to dsDNA structure)
28
Q

What are enhancesomes?

A

Enhancesomes are multiple enhancers that act together on a common promoter

29
Q

How is genetic information selected for trxn into RNA? (just first step)

A

1) A combo of trxn factors bind their specific DNA sequences near promoter
2) if trxn factor is a steroid hormone receptor, once the hormone ligand binds trxn can begin. If hormone is not bound either represses or inactivates trxn
- ENV controls hormone release

30
Q

What is an example of how environmental signals regulate gene expression?

A

-the steroid hormone receptors that activate trxn when hormone is presence and bound and inactivate trxn when hormone is absent

31
Q

What are steroid hormone receptors?

A
  • are protein trxn factors

- bind to the SRE( steroid response element) in DNA and help regulate gene expression

32
Q

SRE?

A
  • steroid response element

- a specific DNA sequence that regulates trxn

33
Q

What is the steroid hormone receptor gene regulation mechanism?

A

1) when hormone (ligand) is present, binds the receptor which removes the co-repressors
2) removal of co-repressors allows co-activators to bind
3) the complex is now active, recruits basal machinery w/ RNA polymerase 2
4) trxn begins

34
Q

What are miRNAs?

A

short, regulatory RNAs that are complimentary to mRNA of genes

  • REGULATE GENE EXPRESSION
  • mostly occurs in 3’ UTR
  • are in a hairpin loop structure
35
Q

How are miRNAs encoded?

A

1) begin as precursor miRNA (pre-miRNA) ~70nt

2) processed into ~21-23nt ss miRNAs

36
Q

How do miRNAs work?

A

(HAIRPIN NEEDS TO BE UNDONE FIRST. won’t bind if in hairpin structure)
-once miRNA binds it’s complement strand in 3’ UTR of mRNA, it represses the translation of that segment of RNA
OR can degrade that segment of RNA therefore silencing it’s translation

37
Q

RNA interference (RNAi)?

A
  • is the use of miRNA to halt translation of a certain protein
  • uses synthetically produced short interfering RNA (siRNA) to bind the desired mRNA sequence
  • can be used therapeutically
38
Q

siRNA vs. miRNA?

A 
siRNA= synthetic 
miRNA= the natural way
39
Q

How are miRNA’s made? What are the key players?

A
  • requires Drosha, Dicer, & RISC complex
  • REQUIRES functional Drosha & dicer
  • these processes make a 22nt single stranded miRNA from a 70nt one
  • can repress translation, can cleave & degrade mRNA
40
Q

What are the 3 ways that miRNAs can regulate protein expression?

A

1) mRNA degradation
2) translational regulation
3) transcriptional regulation via epigenetic mechanism such as histone methylation that silences genes

41
Q

What is epigenetic?

A

epigenetic are HERITABLE changes in patterns of gene expression
-these changes DO NOT alter the primary nucleotide (DNA) sequence

42
Q

What are the mechanism of epigenetic inheritance? What is the key to epigenetic?

A

1) DNA methylation
2) Histone modifications
3) (regulatory non-coding RNAs (miRNAs)

Genes need to be open/accessible to be transcribed

43
Q

How does chromatin play a role in trxn?

A
  • chromatin naturally is less condensed than chromosomes but still squished up so can fit into nucleus
  • chromatin needs to go from condensed–> open state so can be trxn
  • BUT only small segment that wants to be trxn can be unwound, if unwind entire chromatin then will be too huge for cell
  • once chromatin open, then general TF can do their thing
44
Q

How do we regulate the packaging of DNA into condensed state?

A

Through histones

-histones are primary regulatory elements of chromatin structure & therefore gene expression

45
Q

How do we regulate histones?

(3 ways) What do these modifications affect?

A

1) methylation
2) acetylation
3) phosphorylation

  • modifications to histones affect how condensed/open chromatin is therefore regulating gene expression
  • also regulate DNA repair
46
Q

What is histone acetylation? How work?

A
  • acetyl group is added/ removed from lysine
  • acetylation removes + charge from AA
  • makes chromatin OPEN
47
Q

What are the two enzymes involved in histone acetylation?

A

1) HAT: histone acetyltransferase

2) HDAC: histone deacetylase

48
Q

Acetylation vs. Methylation

A

1) Acetylation: increases gene expression
de-actylation: decrease expression
2) methylation: decreases gene expression
de-methylation: increase expression

49
Q

what are HDACs?

A
  • Histone deactylases
  • 18 in human genome, often are in trxn factor complexes
  • have roles in many diseases
50
Q

What are sirtuins?

A
  • HDACs that are NAD+ dependent
  • foods regulate their activity
  • said that wine increases it’s activity and increased activity can increase life span
51
Q

Where does DNA methylation occur? What does methylation do?

A
  • CpG islands

- methylation prohibits transcription of a gene

52
Q

CpG islands?

A
  • cytosine-phosphate-guanine;
  • assocated w/ promoter regions
  • occur in short stretches in mammals, rarely just a dinucleotide
  • place of methylation
  • in norma
53
Q

When/Why are CpG islands methylated?

A
  • NOTmethylated in normal cells
  • methylated when have highly repetitive sequence because this repetition indicates it’s used for chromosome stability or is a remnant of viral pathogens so DO NOT WANT IT TRANSCRIBED
54
Q

If CpG islands are very abundant…what does it suggest?

A

-a prokaryotic genome such as a virus

55
Q

What are other functions of DNA methylation besides epigenetic? (6)

A

1) trxn splicing
2) chromatin compaction
3) genome stability
4) suppression of homologous recombination between repeats
5) genome defense
6) X-chromosome inactivation (Females)

56
Q

What is relationship between Epigenetic & cancer?

A
  • epigenetic changes to the DNA repair genes have been shown to be a major step in early cancer progression
  • HYPERmethylation–> can lead to halting trxn of tumor suppressor genes…therefore allowing proliferation of tumors
57
Q

Hypo OR Hyper DNA methylation cause increase in cancer risk?

A
  • BOTH can depending on which type of gene is affected
  • hypermethylation of tumor suppressor genes= bad while acetylation= good
  • acetylation of oncogene (proliferation gene)= bad, methylation= good
58
Q

Can mutations be reversed? Can epigenetic changes?

A

-mutations can’t, epigenetic changes can with certain therapies such as deactylases

59
Q

Do epigenetic markers change over time? Example?

A

YES

  • epigentic changes are highly subjective to environment and readily change over time
  • identical twins indsitinguishable at young age…remarkable different as age due to env. and life experiences

Block 1 Week 1 (9 decks)

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