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Cheryl M. Tucker

Researcher at Princeton University

Publications -  9
Citations -  1910

Cheryl M. Tucker is an academic researcher from Princeton University. The author has contributed to research in topics: Experimental evolution & Mutation. The author has an hindex of 7, co-authored 9 publications receiving 1723 citations. Previous affiliations of Cheryl M. Tucker include Massachusetts Institute of Technology.

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Effects of Aneuploidy on Cellular Physiology and Cell Division in Haploid Yeast

TL;DR: It is concluded that aneuploidy causes not only a proliferative disadvantage but also a set of phenotypes that is independent of the identity of the individual extra chromosomes.
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The repertoire and dynamics of evolutionary adaptations to controlled nutrient-limited environments in yeast.

TL;DR: This work describes genetic changes that resulted from the experimental adaptation of 24 haploid and diploid cultures of Saccharomyces cerevisiae to growth in either glucose, sulfate, or phosphate-limited chemostats and suggests that experimental evolution can also shed light on the function and regulation of individual metabolic pathways.
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Identification of aneuploidy-tolerating mutations

TL;DR: The results demonstrate the existence of aneuploidy-tolerating mutations that improve the fitness of multiple different aneuPLoidies and highlight the importance of ubiquitin-proteasomal degradation in suppressing the adverse effects of anneuploids.
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Loss of Heterozygosity Drives Adaptation in Hybrid Yeast.

TL;DR: This is an example where hybrid genome resolution is driven by positive selection on existing heterozygosity and demonstrates that even infrequent outcrossing may have lasting impacts on adaptation.
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Fis1 deficiency selects for compensatory mutations responsible for cell death and growth control defects.

TL;DR: It is reported that deletion of the FIS1 gene in yeast consistently results in acquisition of a secondary mutation that confers sensitivity to cell death, which drives the selection for specific compensatory mutations that confer defective growth control and cell death regulation, characteristic of human tumor cells.