Systems approaches identify the consequences of monosomy in somatic human cells

Narendra Kumar Chunduri, Paul Menges, Xiaoxiao Zhang, Angela Wieland, Vincent Leon Gotsmann, Balca R. Mardin, Christopher Buccitelli, Jan O. Korbel, Felix Willmund, Maik Kschischo, Markus Raeschle and Zuzana Storchova ()
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Narendra Kumar Chunduri: TU Kaiserslautern
Paul Menges: TU Kaiserslautern
Xiaoxiao Zhang: University of Applied Sciences Koblenz
Angela Wieland: TU Kaiserslautern
Vincent Leon Gotsmann: TU Kaiserslautern
Balca R. Mardin: European Molecular Biology Laboratory (EMBL)
Christopher Buccitelli: European Molecular Biology Laboratory (EMBL)
Jan O. Korbel: European Molecular Biology Laboratory (EMBL)
Felix Willmund: TU Kaiserslautern
Maik Kschischo: University of Applied Sciences Koblenz
Markus Raeschle: TU Kaiserslautern
Zuzana Storchova: TU Kaiserslautern

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: Abstract Chromosome loss that results in monosomy is detrimental to viability, yet it is frequently observed in cancers. How cancers survive with monosomy is unknown. Using p53-deficient monosomic cell lines, we find that chromosome loss impairs proliferation and genomic stability. Transcriptome and proteome analysis demonstrates reduced expression of genes encoded on the monosomes, which is partially compensated in some cases. Monosomy also induces global changes in gene expression. Pathway enrichment analysis reveals that genes involved in ribosome biogenesis and translation are downregulated in all monosomic cells analyzed. Consistently, monosomies display defects in protein synthesis and ribosome assembly. We further show that monosomies are incompatible with p53 expression, likely due to defects in ribosome biogenesis. Accordingly, impaired ribosome biogenesis and p53 inactivation are associated with monosomy in cancer. Our systematic study of monosomy in human cells explains why monosomy is so detrimental and reveals the importance of p53 for monosomy occurrence in cancer.

Date: 2021
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DOI: 10.1038/s41467-021-25288-x

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