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Exploring the evolutionary rate differences between human disease and non-disease genes.

Sandip Chakraborty1, Arup Panda1, Tapash Chandra Ghosh1

  • 1Bioinformatics Centre, Bose Institute, P-1/12, C.I.T. Scheme VII M, Kolkata 700 054, India.

Genomics
|November 13, 2015
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Summary

Human disease genes, particularly tissue-specific ones, evolve slower than non-disease genes. This slower evolution is linked to higher protein complex numbers and multifunctionality, offering insights into disease genetics.

Keywords:
Disease genesEvolutionary ratesExpression breadthHumanMultifunctionalityProtein complex

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Area of Science:

  • Genomics
  • Evolutionary Biology
  • Human Genetics

Background:

  • Understanding the evolutionary rates of human disease genes is crucial for deciphering their genetic basis.
  • Previous studies have yielded conflicting results regarding whether disease genes evolve faster or slower than non-disease genes.

Purpose of the Study:

  • To resolve the controversy surrounding the evolutionary rates of human disease genes compared to non-disease genes.
  • To investigate factors influencing the evolutionary rate of human disease genes.

Main Methods:

  • Integrated human disease genes from multiple databases.
  • Compared protein evolutionary rates of disease and non-disease genes, categorizing them into housekeeping and tissue-specific groups.
  • Analyzed protein complex number, gene expression levels, and biological process conservation for tissue-specific disease genes.
  • Performed regression analysis to identify factors modulating evolutionary rates.

Main Results:

  • Tissue-specific disease genes exhibit significantly slower evolutionary rates than their non-disease counterparts.
  • No significant difference in evolutionary rates was observed between disease and non-disease genes within the housekeeping group.
  • Tissue-specific disease genes are characterized by higher protein complex numbers, elevated gene expression, and association with conserved biological processes.
  • Protein complex number and protein multifunctionality were identified as independent modulators of human disease gene evolutionary rates.

Conclusions:

  • Evolutionary rates of human disease genes differ based on their functional context (tissue-specific vs. housekeeping).
  • Tissue-specific disease genes evolve slower due to increased functional constraints, such as involvement in larger protein complexes and multifunctionality.
  • Protein complex formation and multifunctionality are key determinants of the evolutionary trajectory of human disease genes.