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Regulation Of Gene Expression > Lesson 4 > Flashcards

Lesson 4 Flashcards

1
Q

What is a psendogene?

A

A genomic locus that resembles real genes but do not have biological relevance / consequence → transduced into RNA but not translated into a protein

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2
Q

How prevalent are pseudogenes?

A

Are almost as numerous as coding genes

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3
Q

Although they lack canonical promoters, what do pseudogenes use to regulate their transcription?

A

Proximal regulatory elements

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4
Q

Describe psendogene transcription in regards to location and presentation:

A

Exhibits tissue-specificity and is aberrantly activated in cancer

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5
Q

What is PTEN?

A

A central gene which is involved in one of the central pathways that is activated in cancer→ resides in the short arm of chromosome 10

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6
Q

Why is PTEN an important tumor suppressor?

A

It blocks AKT→ many tumors eliminate PTEN to activate AKT pathway to induce cancer

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7
Q

What are the 2 main functions of miRNAs?

A

Reduce the levels of RNAs by inducing degradation (catabolism) and to block translation

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8
Q

What is the “sponge effect”?

A

When the psendgogene and the gene go in the same direction → shutting down 1 leads to the reduction of the other

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9
Q

What is the competitive endogenous RNA (ceRNA) hypothesis?

A

Passive players become active players →microRNA from active genes become passive because pseudogenes become sponges for the microRNA and they are trapped in the pseudogene

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10
Q

What are the 2 main DNA repair pathways?

A

Homologous and nonhomologous recombination

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11
Q

Which method of DNA repair is more error-prone?

A

Non-homologous DNA repair

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12
Q

Tumor suppressor genes often have what type of deletions?

A

Heterozygous deletions→ but remaining copy is mutated

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13
Q

How is the expression of a gene effected when a deletion is present?

A

The gene has increased expression

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14
Q

Name four characteristics of pseudogenes:

A
  1. almost as numerous as coding genes
  2. represent a significant portion of the transcriptome
  3. processed pseudogenes use proximal regulator elements to mediate transcription
  4. exhibit tissue-specificity and is aberrantly activated in cancer
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15
Q

What can miRNAs bind to?

A

both the gene itself at the 3’ end and the pseudogene

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16
Q

What must happen in cancer in order to shut down the effect of the tumor suppressor?

A

the elimination of the pseudogene lets the miRNA target PTEN causing PTEN to go down - cancer cell losses PTEN

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17
Q

Describe the sponge effect in regards to PTEN and miRNA in cancer:

A

the pseudogene and the gene go in the same direction → by shutting down one we get the reduction of the other - losing the endogenous sponge the target gene is free to be targeted

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18
Q

In the case of cancer and PTEN, what will happen if the pseudogene is increased?

A

this means increasing the expression of PTEN meaning the cells will grow more slowly (since it is a tumor suppressor)

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19
Q

In what way does the ceRNA hypothesis suppose that passive players become active players?

A

microRNA from active become passive because pseudogenes become sponges for the microRNA and they are trapped by the pseudogene

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20
Q

What do pseudogenes behave like?

A

tumor suppressors and oncogenes

21
Q

How do pseudogenes behave like oncogenes?

A

increase in copy numbers

22
Q

how do pseudogenes behave like tumor suppressors?

A

loss of genome

23
Q

what are fragile site?

A

portions of the genome on which there are some parts that seem to be more fragile than others

24
Q

what happens at fragile sites during mitosis?

A

breakage of these sites of a genome causes small deletions and small amplifications inducing errors

25
Q

what type of DNA repair occurs at fragile sites?

A

non-homologous repair

26
Q

looking at the entire genome, genes residing in fragile sites tend to have what type of expression?

A

downregulated

27
Q

what is the outcome of a focal deletion?

A

a shorter over expressed protein

28
Q

what occurs when a pseudogene is cut out using CRISPR-Cas?

A

losing the pseudogene, the silencer is removed and there is an increase in expression of the corresponding gene → deletion induces expression of a gene

29
Q

what occurs when CRISPR-Cas is bound to the KRAB domain?

A

inactive Cas9 binds in proximity to the promoter and KRAB shuts down the expression of the pseudogene → thus we obtain in increase of the corresponding gene

30
Q

describe the “leaking effect” in CRISPR-Cas 9 domains

A

methylation domains are deposited but the methylation is spread and effects the pseudogene

31
Q

overall, what is a pseudogene?

A

a silencer

32
Q

what effect has been suggested that a pseudogene has on polymerase?

A

RNA polymerase stops when it finds a pseudogene

33
Q

experiments show that during mitosis there is genomic instability and chromosomic instability in patients, how could we treat this issue?

A

with kinase inhibitors

34
Q

what two groups are non-coding RNAs divided into?

A

below 200 nt and above 200 nt

35
Q

what are non-coding RNAs above 200 nt called?

A

long non-coding RNAs (lncRNA) or long non-coding intergenic RNAs (lincRNA)

36
Q

describe the differences between mRNA and lncRNAs:

A
  1. tend to be shorter
  2. fewer but longer exons
  3. expressed at relatively low levels
  4. have poorer primary sequence conservation
37
Q

what two histone markers can be used to find lncRNA?

A

H3K4me3 and H3K36me3

38
Q

where are lncRNA expressed?

A

each tissue has a very specific set of lncRNA that is only expressed in that specific tissue

39
Q

where are encoding genes expressed?

A

all tissues

40
Q

compare the expression of lncRNAs and encoding genes:

A

lncRNAs present a lower median expression but they have much higher tissue specificity

41
Q

where do pseudogenes tend to be located?

A

in the nucleus

42
Q

what are the two phenotypic outcomes of the activation of the p53 pathway?

A

growth arrest and apoptosis - suggesting that lincRNAs can mediate this pathway

43
Q

what happens in tumors, sarcomas and lymphoma if we put back p53?

A

there is a lot of increase on the RNA level of p21

44
Q

what is PANDA?

A

a gene repressor that induces apoptosis and compensates the action of p53

45
Q

what is the function of DINOL?

A

close to p21, stabilized p53 and modulates the activity of its target genes - if there isn’t DINOL we have a down-regulation of p53

46
Q

what do lncRNAs act in?

A

chromatin interactions (can form a loop with different portions of the DNA), protein interactions, and RNA interactions

47
Q

What is the target of p53 when it is activated?

A

p21

48
Q

when is p53 activated?

A

after DNA damage

Regulation Of Gene Expression (28 decks)

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