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Year 3: SGE > Transposable elements > Flashcards

Transposable elements Flashcards

1
Q

How big are TEs usually?

A

1-3kb

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2
Q

They can have a) moderate and b) high levels of repeats. How long are these?

A

a) 1-100 repeats

b) 1 million

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3
Q

Are TEs dispersed across the genome?

A

Yes

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4
Q

Are TEs mobile?

A

Yes

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5
Q

TEs cannot replicate. True or false?

A

False

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6
Q

There are 2 types of TE. What is a retrotransposon?

A

TEs that use reverse transcriptase to generate cDNA (behave like retroviruses)

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7
Q

Describe how retrotransposons replicate.

A

Transcription of DNA to RNA.
Reverse transcription of RNA to cDNA.
Incorporation of cDNA by integrase.

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8
Q

There are 2 types of TE. What is a DNA element?

A

TEs that transpose as DNA with no RNA intermediate

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9
Q

Describe how DNA elements replicate.

A

‘Cut and paste’ approach:
Transposase enzyme cuts TE free, producing a sticky end.
TE ligates to new target site.
DNA polymerase fills in the gaps.
Ligase closes the sugar-phosphate backbone.

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10
Q

Transposition is good for the element. Why is it beneficial before meiosis?

A

TE copies itself onto both sister chromatids of a chromosome before they segregate, means it ends up in 50% of the gametes.

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11
Q

Transposition is good for the element. Why is it beneficial during meiosis?

A

TE transposes from one chromosome onto another that is NOT its homologue (presumably bc they are all lined up in close proximity). If it has already copied itself onto sister chromatids of the original, will end up in 75% of the gametes.

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12
Q

Give 3 major costs of TEs for the host.

A
  1. Expensive to produce extra DNA/RNA/proteins for transposition
  2. Major risk of spontaneous mutation, most of which deleterious
  3. Ectopic recombination as it causes non-homologous pairings at meiosis, causes unbalanced chromsomes
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13
Q

In terms of TEs, what is individual selection?

A

Competition on each TE individually, causes competition between TEs

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14
Q

In terms of TEs, what is group selection?

A

Competition between hosts

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15
Q

Individual selection favours TEs with what?

A

Higher transposition rates

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16
Q

Group selection favours what?

A

Hosts with fewer TEs

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17
Q

Individual and group selection are antagonistic. True or false?

A

True.

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18
Q

Are ‘groups’ permanent?

A

No bc host genomes are constantly broken up by recombination

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19
Q

The Drosophila view of TEs:

What happens to TEs that insert into exons?

A

They are removed by selection as disrupt gene function

20
Q

The Drosophila view of TEs:

So where do TEs accumulate and why?

A

In introns, so areas of low gene density and low recombination, bc selection is weaker in these regions.

21
Q

The Drosophila view of TEs:

Give examples of areas of low recombination.

A

Y chromosome, inversions etc.

22
Q

Harm that results from TEs increases exponentially with copy number. Why?

A

Because TEs increase the likelihood of ectopic recombination.

23
Q

The Drosophila view of TEs:

What did Petrov (2011) investigate in D. melanogaster?
What did they find?
What did they conclude?

A

Looked at whether the most damage from TEs came from insertion of the TE or ectopic recombination.

Look at 70+ strains.
Found over 755 different TEs.
None were found in exons, implies strong purifying selection.
All TEs found in introns.
TEs v. rare in areas of high recombination.

Ectopic recombination causes more damage

24
Q

The Drosophila view of TEs:

What evidence did Petrov (2011) find for the theory that TEs cause ectopic recombination?

What

A
  1. Long TEs are rare as increases chance of ectopic recombination.
  2. High copy number of TEs v. rare per site, as increases likelihood of ectopic recombination
  3. No association of TE with distance from coding region, as if was close to coding region then would disrupt regulatory sequences
25
Q

Hosts can develop repression mechanisms against TEs. Who described P elements in D. melanogaster?

A

Khurana et al. (2011)

26
Q

Khurana et al., 2011:

Piwi proteins associate with different piRNAs. Each piRNA associates with a different transposon. In D. melanogaster which transposons do Piwi proteins associate with?

WT females repress P elements. How?

How did the authors discover this?

What is hybrid dysgenesis?

If you mate WT females with lab males, what can be said of the offspring?

Why do WT drosophila have p elements and lab strains do not?

A

P elements

They have piRNA and Piwi proteins in their cytoplasm.

They mated WT males (p elements with no repression) and lab females (no p elements), F1 displayed hybrid dysgenesis.

High mutation rates and sterility due to an explosion of P elements

F1 are fine bc have inherited repression along with p elements from mother

Lab strains were isolated before the invasion of the p element.

27
Q

Khurana et al. (2011):

Why is the P element self-limiting?

A

P is self limiting as it causes male infertility in hybrids (between P male and lab female) and hybrid dysgenesis

28
Q

Khurana et al. (2011):

What happens to male infertility as males age? Why?

A

They become fertile as they age as the piRNA machinery assembles and they acquire ‘immunity’ to the P elements

29
Q

Khurana et al. (2011):

What is piRNA?

A

Small, anti-sense TE fragments

30
Q

Khurana et al. (2011):

Where is piRNA stored?

A

In centromeric heterochromatin

31
Q

Khurana et al. (2011):

What does piRNA do?

A

Binds to TEs

32
Q

Who described one mechanism of the Piwi system?

A

Brennicke et al., 2007

33
Q

Brennicke et al., 2007:

Outline how the Ping Pong cycle works as outlined by the authors.

A

Aubergine protein is associated w/ antisense piRNA

Antisense piRNA binds TE, flags it for destruction

Aubergine releases piRNA

Argonaute associated w/ sense strand of piRNA

Argonaute synthesises antisense piRNA

This piRNA used to replenish Aubergine

Cycle called Ping Pong as it constantly goes back and forth

34
Q

The Piwi system is a set of proteins associated with piRNAs. What can it be described as?

A

‘Genetic memory’ of TEs, like an immune system within the genome.

35
Q

Does selection always favour TEs with high transposition rates?

A

No

36
Q

Why doesn’t selection always favour TEs with high transposition rates?

A

High transposition rate damages the host. In bacteria hosts are asexual and produce clones. This produces a conflict between individual and group selection (as all hosts are identical), thus TE wants to lower transposition rates

37
Q

Hosts can evolve self-repression mechanisms. Who looked at the TE tn10 in E. coli?

How often does it transpose?

What is the IS10 element of the tn10 TE?

A

Kleckner, 1990:

Only transposes every 1000th cell division

IS10 = encodes functional transposase

38
Q

Kleckner (1990):

What are the two mechanisms behind low transposition of the tn10 element in E. coli?

A
  1. TE is methylated.

2. Anti-sense RNA inhibitor binds transposase transcripts of IS10 element to prevent translation of an active enzyme.

39
Q

Kleckner (1990):

What evidence is there that a) methylation and b) anti-sense inhibition of transposase are the repression mechanisms?

A

a) remove methylation and transposition increases 100x
b) inhibition increases exponentially with copy number; more inhibitor produced = more IS10 transcripts prevented from translating

40
Q

TEs can contain LTRs. What are they?

A

Long terminal repeats (basically repeats at the end of DNA sequences)

41
Q

The accumulation of TEs is common. Give a referenced example.

Why is it thought TEs were allowed to accumulate by selection?

A

San Miguel et al. (1998)

Looked specifically at TEs near the adh1 gene in maize

Maize genome found to have doubled over last 3mya from 1200Mb to 2400Mb due to LTRs.

This has been allowed to accumulate by selection as LTRs insert into other LTRs, neutral effect.

42
Q

In the 1960s Barbara McClintock proposed a hypothesis for the retention of TEs. What was it?

A

They are co-opted for gene regulation

43
Q

What evidence is there for co-option of TEs by the host? Give a referenced example (review paper).

A

Gifford et al. (2013), REVIEW

env protein from retroTE in several mammalian lineages mediates cell-cell fusion of the placenta, co-opted to make syncytin

44
Q

Who described co-option of the TE evr1 in regulation of oct4, a major developmental gene?

Oct4 has many names. What is another name for oct4 in humans?

A

Kunarso et al., 2010

POU5F1 in humans

45
Q

Khurana et al., 2011:

After the P elements invade D. melanogaster and produce male infertility, in a few generations male fertility is restored. Why?

A

Males gain fertility back as they age as Piwi machinery assembles. Resident TEs insert into piRNA clusters, leading to the formation of novel piRNAs. These are transmitted to progeny, and associated with reduced transposition.

‘P elements triggers genomic change that induces TE silencing’

Year 3: SGE (11 decks)

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