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Role of duplicate genes in genetic robustness against null mutations

Author

Listed:
  • Zhenglong Gu

    (University of Chicago)

  • Lars M. Steinmetz

    (Stanford University School of Medicine)

  • Xun Gu

    (Iowa State University)

  • Curt Scharfe

    (Stanford University School of Medicine)

  • Ronald W. Davis

    (Stanford University School of Medicine)

  • Wen-Hsiung Li

    (University of Chicago)

Abstract

Deleting a gene in an organism often has little phenotypic effect1,2,3,4,5, owing to two mechanisms of compensation4,5,6,7,8,9,10. The first is the existence of duplicate genes: that is, the loss of function in one copy can be compensated by the other copy or copies. The second mechanism of compensation stems from alternative metabolic pathways, regulatory networks, and so on. The relative importance of the two mechanisms has not been investigated except for a limited study, which suggested that the role of duplicate genes in compensation is negligible10. The availability of fitness data for a nearly complete set of single-gene-deletion mutants of the Saccharomyces cerevisiae genome11 has enabled us to carry out a genome-wide evaluation of the role of duplicate genes in genetic robustness against null mutations. Here we show that there is a significantly higher probability of functional compensation for a duplicate gene than for a singleton, a high correlation between the frequency of compensation and the sequence similarity of two duplicates, and a higher probability of a severe fitness effect when the duplicate copy that is more highly expressed is deleted. We estimate that in S. cerevisiae at least a quarter of those gene deletions that have no phenotype are compensated by duplicate genes.

Suggested Citation

  • Zhenglong Gu & Lars M. Steinmetz & Xun Gu & Curt Scharfe & Ronald W. Davis & Wen-Hsiung Li, 2003. "Role of duplicate genes in genetic robustness against null mutations," Nature, Nature, vol. 421(6918), pages 63-66, January.
    • Handle: RePEc:nat:nature:v:421:y:2003:i:6918:d:10.1038_nature01198
    DOI: 10.1038/nature01198
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    Cited by:

    1. Alon Kaufman & Alon Keinan & Isaac Meilijson & Martin Kupiec & Eytan Ruppin, 2005. "Quantitative Analysis of Genetic and Neuronal Multi-Perturbation Experiments," PLOS Computational Biology, Public Library of Science, vol. 1(6), pages 1-7, November.
    2. Fadi J. Najm & Peter DeWeirdt & Molly M. Moore & Samantha M. Bevill & Chadi A. El Farran & Kevin A. Macias & Mudra Hegde & Amanda L. Waterbury & Brian B. Liau & Peter Galen & John G. Doench & Bradley , 2023. "Chromatin complex dependencies reveal targeting opportunities in leukemia," Nature Communications, Nature, vol. 14(1), pages 1-10, December.
    3. Andras Gyorgy, 2023. "Competition and evolutionary selection among core regulatory motifs in gene expression control," Nature Communications, Nature, vol. 14(1), pages 1-12, December.
    4. Ki-Hong Jung & Jinwon Lee & Chris Dardick & Young-Su Seo & Peijian Cao & Patrick Canlas & Jirapa Phetsom & Xia Xu & Shu Ouyang & Kyungsook An & Yun-Ja Cho & Geun-Cheol Lee & Yoosook Lee & Gynheung An , 2008. "Identification and Functional Analysis of Light-Responsive Unique Genes and Gene Family Members in Rice," PLOS Genetics, Public Library of Science, vol. 4(8), pages 1-19, August.
    5. Joseph Bozorgmehr, 2012. "Natural selection as a paradigm of opportunism in biology," Journal of Bioeconomics, Springer, vol. 14(1), pages 61-75, April.
    6. Malaguti, Giulia & Singh, Param Priya & Isambert, Hervé, 2014. "On the retention of gene duplicates prone to dominant deleterious mutations," Theoretical Population Biology, Elsevier, vol. 93(C), pages 38-51.

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