ArticleThe EMBO journal2021
Epistasis, aneuploidy, and functional mutations underlie evolution of resistance to induced microtubule depolymerization.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Resolving translational challenges in cancer biology through yeast experimental evolution.Cancer metastasis reviews · 2026Review
- Combinatorial effects of multiple genes contribute to beneficial aneuploidy phenotypes.EMBO reports · 2026Article
- Inducible chromosomal rearrangement reveals nonlinear polygenic dosage effects in driving aneuploid yeast traits.Nature communications · 2025Article
- Compensatory evolution to DNA replication stress is robust to nutrient availability.Molecular systems biology · 2025Article
- Evolutionary adaptation to hyperstable microtubules selectively targets tubulins and is empowered by the spindle assembly checkpoint.Cell reports · 2025Article
- Experimental evolution for cell biology.Trends in cell biology · 2023Review
- Copy number variation alters local and global mutational tolerance.Genome research · 2023Article
- Long-term evolution of proliferating cells using the eVOLVER platform.Open biology · 2023Article
- Long-term evolution of proliferating cells using the eVOLVER platform.bioRxiv : the preprint server for biology · 2023Article
- Adaptation to high rates of chromosomal instability and aneuploidy through multiple pathways in budding yeast.The EMBO journal · 2023Article
- A fitness trade-off explains the early fate of yeast aneuploids with chromosome gains.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Epistasis, aneuploidy, and functional mutations underlie evolution of resistance to induced microtubule depolymerization.The EMBO journal · 2021Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells with blocked microtubule polymerization are delayed in mitosis, but eventually manage to proliferate despite substantial chromosome missegregation. While several studies have analyzed the first cell division after microtubule depolymerization, we have asked how cells cope long-term with microtubule impairment. We allowed 24 clonal populations of yeast cells with beta-tubulin mutations preventing proper microtubule polymerization, to evolve for ˜150 generations. At the end of the laboratory evolution experiment, cells had regained the ability to form microtubules and were less sensitive to microtubule-depolymerizing drugs. Whole-genome sequencing identified recurrently mutated genes, in particular for tubulins and kinesins, as well as pervasive duplication of chromosome VIII. Recreating these mutations and chromosome VIII disomy prior to evolution confirmed that they allow cells to compensate for the original mutation in beta-tubulin. Most of the identified mutations did not abolish function, but rather restored microtubule functionality. Analysis of the temporal order of resistance development in independent populations repeatedly revealed the same series of events: disomy of chromosome VIII followed by a single additional adaptive mutation in either tubulins or kinesins. Since tubulins are highly conserved among eukaryotes, our results have implications for understanding resistance to microtubule-targeting drugs widely used in cancer therapy.
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