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Dynamics of age-related catastrophic mitotic failures and recovery in yeast

View ORCID ProfileMatthew M. Crane, Adam E. Russell, Brent J. Schafer, Mung Gi Hong, Joslyn E. Goings, Kenneth L. Chen, Ben W. Blue, View ORCID ProfileMatt Kaeberlein
doi: https://doi.org/10.1101/466797
Matthew M. Crane
1Department of Pathology, University of Washington, Seattle, WA, USA
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  • For correspondence: mcrane2@uw.edu kaeber@uw.edu
Adam E. Russell
1Department of Pathology, University of Washington, Seattle, WA, USA
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Brent J. Schafer
1Department of Pathology, University of Washington, Seattle, WA, USA
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Mung Gi Hong
1Department of Pathology, University of Washington, Seattle, WA, USA
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Joslyn E. Goings
1Department of Pathology, University of Washington, Seattle, WA, USA
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Kenneth L. Chen
1Department of Pathology, University of Washington, Seattle, WA, USA
2Department of Genome Sciences, University of Washington, Seattle, Washington, USA
3Medical Scientist Training Program, University of Washington, Seattle, Washington USA
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Ben W. Blue
1Department of Pathology, University of Washington, Seattle, WA, USA
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Matt Kaeberlein
1Department of Pathology, University of Washington, Seattle, WA, USA
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  • ORCID record for Matt Kaeberlein
  • For correspondence: mcrane2@uw.edu kaeber@uw.edu
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Abstract

Genome instability is a hallmark of aging and contributes to age-related disorders such as progeria, cancer, and Alzheimer’s disease. In particular, nuclear quality control mechanisms and cell cycle checkpoints have generally been studied in young cells and animals where they function optimally, and where genomic instability is low. Here, we use single cell imaging to study the consequences of increased genomic instability during aging, and identify striking age-associated genome missegregation events. During these events the majority of mother cell chromatin, and often both spindle poles, are mistakenly sent to the daughter cell. This breakdown in mitotic fidelity is accompanied by a transient cell cycle arrest that can persist for many hours, as cells engage a retrograde transport mechanism to return chromosomes to the mother cell. The repetitive ribosomal DNA (rDNA) has been previously identified as being highly vulnerable to age-related replication stress and genomic instability, and we present several lines of evidence supporting a model whereby expansion of rDNA during aging results in nucleolar breakdown and competition for limited nucleosomes, thereby increasing risk of catastrophic genome missegregation.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted November 09, 2018.
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Dynamics of age-related catastrophic mitotic failures and recovery in yeast
Matthew M. Crane, Adam E. Russell, Brent J. Schafer, Mung Gi Hong, Joslyn E. Goings, Kenneth L. Chen, Ben W. Blue, Matt Kaeberlein
bioRxiv 466797; doi: https://doi.org/10.1101/466797
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Dynamics of age-related catastrophic mitotic failures and recovery in yeast
Matthew M. Crane, Adam E. Russell, Brent J. Schafer, Mung Gi Hong, Joslyn E. Goings, Kenneth L. Chen, Ben W. Blue, Matt Kaeberlein
bioRxiv 466797; doi: https://doi.org/10.1101/466797

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