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Multimerization variants as potential drivers of neofunctionalization.

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Genetic redundancy from whole-genome duplications allows for new cellular functions. Protein complex size variations commonly drive gene neofunctionalization, impacting diverse protein classes.

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Area of Science:

  • Evolutionary biology
  • Molecular biology
  • Proteomics

Background:

  • Whole-genome duplications (WGDs) are key evolutionary events providing genetic redundancy.
  • This redundancy can facilitate the emergence of novel cellular functions and protein-protein interactions.
  • However, the role of protein complex variability in driving gene neofunctionalization remains underexplored at a proteome-wide scale.

Purpose of the Study:

  • To investigate the extent to which variations in protein complex formation contribute to neofunctionalization.
  • To identify instances where changes in protein complex size have occurred during evolution.
  • To understand the link between genetic redundancy, protein complex dynamics, and functional diversification.

Main Methods:

  • Utilized protein correlation profiling to analyze apparent mass variations in thousands of orthologous proteins.
  • Compared protein complexes across diverse species and cell types.
  • Examined evolutionary histories, including whole-genome duplication and allopolyploidy events.

Main Results:

  • Variations in protein complex size were frequently observed across different species and cell types.
  • These size variants were often associated with recent whole-genome duplications or allopolyploidy events.
  • Examples, such as carbonic anhydrase orthologs, showed neofunctionalization of ancient paralogs linked to complex size changes.
  • Homo- and heteromer formation were identified as significant drivers of neofunctionalization.

Conclusions:

  • Protein complex size variability is a common evolutionary mechanism.
  • Changes in homo- and heteromer formation can drive neofunctionalization across various protein classes, including enzymes, signaling, and structural proteins.
  • This study highlights a crucial pathway for functional diversification enabled by genetic redundancy.