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Aneuploidy confers quantitative proteome changes and phenotypic variation in budding yeast

Author

Listed:
  • Norman Pavelka

    (Stowers Institute for Medical Research)

  • Giulia Rancati

    (Stowers Institute for Medical Research)

  • Jin Zhu

    (Stowers Institute for Medical Research)

  • William D. Bradford

    (Stowers Institute for Medical Research)

  • Anita Saraf

    (Stowers Institute for Medical Research)

  • Laurence Florens

    (Stowers Institute for Medical Research)

  • Brian W. Sanderson

    (Stowers Institute for Medical Research)

  • Gaye L. Hattem

    (Stowers Institute for Medical Research)

  • Rong Li

    (Stowers Institute for Medical Research
    University of Kansas Medical Center)

Abstract

Positive effects of aneuploidy Aneuploidy, the presence of an abnormal number of chromosomes, has been associated with developmental defects and cancer, but also with adaptive evolution in experimental organisms. Recent studies raised doubts over whether aneuploidy affects gene expression at the proteome level or whether it can bring phenotypic variation and improved fitness over euploid counterparts. A profiling study of a large set of aneuploid yeast strains grown under a variety of conditions demonstrates that aneuploidy can affect both the transcriptome and the proteome, and generate significant phenotypic variation that can lead to fitness gains.

Suggested Citation

  • Norman Pavelka & Giulia Rancati & Jin Zhu & William D. Bradford & Anita Saraf & Laurence Florens & Brian W. Sanderson & Gaye L. Hattem & Rong Li, 2010. "Aneuploidy confers quantitative proteome changes and phenotypic variation in budding yeast," Nature, Nature, vol. 468(7321), pages 321-325, November.
  • Handle: RePEc:nat:nature:v:468:y:2010:i:7321:d:10.1038_nature09529
    DOI: 10.1038/nature09529
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    Cited by:

    1. Rong Xiao & Deshu Xu & Meili Zhang & Zhanghua Chen & Li Cheng & Songjie Du & Mingfei Lu & Tonghai Zhou & Ruoyan Li & Fan Bai & Yue Huang, 2024. "Aneuploid embryonic stem cells drive teratoma metastasis," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    2. Fabio Alfieri & Giulio Caravagna & Martin H. Schaefer, 2023. "Cancer genomes tolerate deleterious coding mutations through somatic copy number amplifications of wild-type regions," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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