Transposable Elements Flashcards

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1
Q

class 2 TEs

A

DNA elements

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2
Q

DNA TE’s

A

cut and paste method

  • transposition through DNA intermediate: element excises and reinserts elsewhere in genome
  • autonomous elements- code for transposase
  • non-autonomous- do not code for transposase
  • terminal inverted repeats
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3
Q

first DNA TEs recognized

A

activator (AC) autonomous

dissociation (DS) non autonomous in maize

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4
Q

MITEs

A

minature inverted repeat transposable elements

  • small, non-autonomous DNA elements
  • found near genes (unlike other transposons)
  • very high copy number
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5
Q

DNA TE gene mobility

A

can capture and mobilize genes and gene fragments
sometimes contain gene fragments
many non-functional pseudogenes
- some are expressed and show few signatures of selection
– low ka/ks values, no frameshifts or INDELs
— suggests some are functional

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6
Q

class 1 TEs

A

RNA elements

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7
Q

RNA TEs

A
class 1: retrotransposons
copy and paste
- mRNA is transposon intermediate
- usually high copy number
A: LTR Retrotransposons
- replicative retroposition
- direct orientation terminal repeats
B: NON- LTR retrotransposons
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8
Q

LTR retrotransposons

A

long terminal repeats in DIRECT orientation
- gag and pol coding regions
- gag codes for capsid like proteins
- pol polyprotein codes for RT, protease, RNaseH, integrase
- LOCATION:
Nucleus, RT in cytoplasm, cDNA transport to nucleus

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9
Q

Non-LTR retrotransposons

A
most prevalent type in human genome
- NO terminal repeats
- LINEs ( ORF1, EN, RT ORFs)
- SINEs (short intersperced nuclear elements)
-- no coding regions
- LOCATION:
nucleus, priming and RT at target site
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10
Q

LINEs/SINEs

A

long/short interspersed nuclear elements

  • LINES: autonomous
  • SINEs: non-autonomous, no coding regions
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11
Q

effects of TEs that insert into genes

A
  1. insertional mutagenesis
    - insert into exon
    - insert into enhancer
    - insert into repressor
  2. Epigenetic regulation
    - antisense downregulation
    - - inserts into 3’ region and makes antisense RNA to form dsRNA– rna degraded and downregulated
    - epigenetic silencing
    - - metalation of transposon to prevent proliferation
  3. Introduction of new information
    - TEs bring new enhancers/ repressors
    - TEs introduce new splice sites
    - TEs bring new promoter or start site
  4. Transduction!
    - introduce new exon into gene
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12
Q

transduction

A

intro of new exon into a gene by TEs

  • 5’: 5’ end exon of gene incorporated
  • 3’
  • premature polyadenylation if TE has polyadenylation signal in it
    • premature polyadenylation of protein
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13
Q

Nested Retrotransposons

A
  • transposons inserted into other transposons
  • each retrotransposon originated later than DNA flanking it
  • leads to increased distance btw genes and increased genome size
  • diagram ones closest to top newest
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14
Q

Dating Transposons

A

LTR dating

  • for non nested transposons
  • LTRs are same upon insertion then diverge
  • LTR divergence indicates age of insertion
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15
Q

families of TEs

A

phylogenetic analysis of autonomous TEs based on Open Reading frames within TE

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16
Q

epigenetic silencing of transposons

A

transcriptional silencing
- methylation of TE promoters
- chromatin remodeling
post-translational silencing: sequence specific RNA degradation
- double stranded RNA, formed by readthrough transcription from neighboring gene
– inverse of antisense degradation
- siRNAs: target TEs for degradation

17
Q

siRNA

A

small interfering RNAs

  • silence retrotransposons
  • dsRNA of retrotransposon triggers Dicer mediated siRNA
  • antisense siRNA binds TE mRNA and degrades
18
Q

TE variation and diversity

A

genome size not related to complexity
More basal= More TE diversity
- most organisms are LINE TE classes

19
Q

Types of TE in human geneome

A

45% og genome are TEs
most are LINES
except ALU which is a SINE
- only non-LTR TEs are active

20
Q

DNA transposons and human genome

A

least common - cut and paste method so not as much gene copy numbers

21
Q

TE balance btw expression and repression

A

expression should be sufficent to promote amplification but not so much that leads to fitness disadvantage for host

22
Q

3 ways TEs can be damaging without transposition

A
  1. TE may interfere with transcriptional processing of host mRNAs if become reactivated
  2. TE encoded proteins can induce DNA breaks+ genomic instability
  3. accumulate RNA transcripts and extrachromosomal DNA copies derived from TEs may trigger innate immunity response
23
Q

how can TEs add exons to genes

A

transduction

- cryptic splice sites which can cause alternative splicing

24
Q

How can TEs provide the building blocks of cis-regulatory networks

A

contain all features of classical gene: integrate multiple inputs, respond to signals and are capable of coordinating regulating gene expression