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Exon Recombination02:32

Exon Recombination

The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
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An exon splice enhancer primes IGF2:IGF2R binding site structure and function evolution.

Christopher Williams1, Hans-Jürgen Hoppe, Dellel Rezgui

  • 1Department of Organic and Biological Chemistry, School of Chemistry, University of Bristol, Bristol BS8 1TS, UK.

Science (New York, N.Y.)
|December 1, 2012
PubMed
Summary
This summary is machine-generated.

Genomic imprinting and placental development evolved due to parental conflict. The evolution of exon splice enhancers in monotremes unexpectedly enabled IGF2R to bind IGF2, initiating this conflict.

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Area of Science:

  • Evolutionary biology
  • Genetics
  • Developmental biology

Background:

  • Placental development and genomic imprinting are linked to parental conflict over offspring resource allocation.
  • The imprinted genes IGF2 and IGF2R regulate growth (IGF2) and its inhibition (IGF2R).
  • IGF2R in non-mammals does not recognize IGF2, unlike in monotremes where IGF2 binds IGF2R via a CD loop.

Purpose of the Study:

  • To investigate the evolutionary origins of IGF2 binding by IGF2R.
  • To understand the role of structural changes in binding affinity.
  • To explore the link between exon splice enhancer (ESE) evolution and the onset of genomic imprinting.

Main Methods:

  • Comparative genomic analysis.
  • Structural modeling of protein-ligand interactions.
  • Analysis of DNA sequences and their functional roles.

Main Results:

  • In monotremes, the DNA coding the IGF2R CD loop acts as an exon splice enhancer (ESE).
  • Structural modifications in binding loops (AB, HI, FG) enhanced IGF2 binding affinity in therian mammals.
  • ESE evolution is proposed to have led to the initial, fortuitous binding of IGF2 by IGF2R.

Conclusions:

  • The evolution of ESEs in monotremes likely facilitated the initial interaction between IGF2 and IGF2R.
  • This interaction may have drawn IGF2R into the parental conflict driving genomic imprinting.
  • Subsequent imprinting could have accelerated the maturation of IGF2R's affinity for IGF2.