10.5061/DRYAD.65364
Torres, Eduardo M.
University of Massachusetts Medical School
Dephoure, Noah
Harvard Medical School
Hwang, Sunyoung
University of Massachusetts Medical School
O’Sullivan, Ciara
Massachusetts Institute of Technology
Dodgson, Stacie E.
Massachusetts Institute of Technology
Gygi, Steve P.
Harvard Medical School
Amon, Angelika
Howard Hughes Medical Institute
Massachusetts Institute of Technology
O'Sullivan, Ciara
University of Massachusetts Medical School
Data from: Quantitative proteomic analysis reveals posttranslational
responses to aneuploidy in yeast
Dryad
dataset
2015
Proteomics
Aneuploidy
2015-07-31T00:00:00Z
2015-07-31T00:00:00Z
en
https://doi.org/10.7554/eLife.03023
7423774 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
Aneuploidy causes severe developmental defects and is a near universal
feature of tumor cells. Despite its profound effects, the cellular
processes affected by aneuploidy are not well characterized. Here, we
examined the consequences of aneuploidy on the proteome of aneuploid
budding yeast strains. We show that although protein levels largely scale
with gene copy number, subunits of multi-protein complexes are notable
exceptions. Posttranslational mechanisms attenuate their expression when
their encoding genes are in excess. Our proteomic analyses further
revealed a novel aneuploidy-associated protein expression signature
characteristic of altered metabolism and redox homeostasis. Indeed
aneuploid cells harbor increased levels of reactive oxygen species (ROS).
Interestingly, increased protein turnover attenuates ROS levels and this
novel aneuploidy-associated signature and improves the fitness of most
aneuploid strains. Our results show that aneuploidy causes alterations in
metabolism and redox homeostasis. Cells respond to these alterations
through both transcriptional and posttranscriptional mechanisms.
Figure 1-Source Data 1TMT and SILAC proteomeTable S1.xlsxFigure 2-Source
Data 1Transcriptome of aneuploid cellsTable S2.xlsxFigure 3-Source Data
1Footprinting of disome VTable S3.xlsxFigure 5-Source Data 1Macromolecular
Complexes in aneuploid cellsTable S4b.xlsxFigure 6-Source Data 1Aneuploid
protein responseTable S5.xlsxFigure 7-Source Data 1Proteome of disomes
harboring the UBP6 deletionTable S6.xlsxFigure 8-Source Data 1Strains
utilizedTable S7.xlsxFigure 4-Source Data 1Protein abundance of WT, disome
II and disome V upon inhibition of protein turnover pathwaysSource Data
4.xlsx