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How big are TEs usually?



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

a) 1-100 repeats
b) 1 million


Are TEs dispersed across the genome?



Are TEs mobile?



TEs cannot replicate. True or false?



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

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


Describe how retrotransposons replicate.

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


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

TEs that transpose as DNA with no RNA intermediate


Describe how DNA elements replicate.

'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.


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

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


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

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.


Give 3 major costs of TEs for the host.

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


In terms of TEs, what is individual selection?

Competition on each TE individually, causes competition between TEs


In terms of TEs, what is group selection?

Competition between hosts


Individual selection favours TEs with what?

Higher transposition rates


Group selection favours what?

Hosts with fewer TEs


Individual and group selection are antagonistic. True or false?



Are 'groups' permanent?

No bc host genomes are constantly broken up by recombination


The Drosophila view of TEs:

What happens to TEs that insert into exons?

They are removed by selection as disrupt gene function


The Drosophila view of TEs:

So where do TEs accumulate and why?

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


The Drosophila view of TEs:

Give examples of areas of low recombination.

Y chromosome, inversions etc.


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

Because TEs increase the likelihood of ectopic recombination.


The Drosophila view of TEs:

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

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


The Drosophila view of TEs:

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


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


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

Khurana et al. (2011)


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?

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.


Khurana et al. (2011):

Why is the P element self-limiting?

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


Khurana et al. (2011):
What happens to male infertility as males age? Why?

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


Khurana et al. (2011):
What is piRNA?

Small, anti-sense TE fragments


Khurana et al. (2011):
Where is piRNA stored?

In centromeric heterochromatin