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Related Experiment Video

Updated: Apr 11, 2026

Saccharomyces cerevisiae Metabolic Labeling with 4-thiouracil and the Quantification of Newly Synthesized mRNA As a Proxy for RNA Polymerase II Activity

Saccharomyces cerevisiae Metabolic Labeling with 4-thiouracil and the Quantification of Newly Synthesized mRNA As a Proxy for RNA Polymerase II Activity

Published on: October 22, 2018

Global stabilization of the transcriptome in mitotic cells.

Ekaterina Khalizeva^1,2, Arash Latifkar^1,2,3, Kehui Xiang^1,2,3

¹Whitehead Institute for Biomedical Research, Cambridge, MA, USA.

The EMBO Journal

|April 9, 2026

Summary

Mammalian cells stabilize their transcriptome during prolonged mitotic arrest, increasing mRNA half-lives over fourfold. This crucial adaptation, dependent on PABPC1&4, prevents mRNA depletion without new transcription, ensuring cell viability.

Keywords:

Deadenylation Gene Regulation Mitosis mRNA Stability

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Last Updated: Apr 11, 2026

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Published on: March 4, 2020

Area of Science:

Molecular Biology
Cell Biology
Genetics

Background:

Cell division errors can cause prolonged mitotic arrest in mammalian cells.
Mitosis requires continued translation for viability despite minimal transcription.
Maintaining mRNA levels during mitotic arrest necessitates adaptations in gene expression.

Purpose of the Study:

To investigate how mammalian cells maintain their transcriptome during extended mitotic delays.
To identify the mechanisms responsible for mRNA stability during mitosis.
To determine the role of specific proteins in mitotic mRNA homeostasis.

Main Methods:

Measurement of mRNA half-lives in interphase versus mitotic arrest.
Analysis of poly(A) tail-length dynamics during mitosis.
Assessment of siRNA-mediated mRNA degradation during mitotic arrest.
Depletion of PABPC1&4 using siRNA and subsequent analysis of mRNA stability and mitotic arrest.

Main Results:

Global stabilization of the transcriptome during prolonged mitotic arrest was observed.
Median mRNA half-lives increased more than fourfold during mitotic arrest compared to interphase.
Mitotic arrest induced changes in poly(A) tail length, suggesting repressed deadenylation.
siRNA-directed mRNA degradation machinery remained active during mitotic arrest.
Depletion of PABPC1&4 compromised mRNA stability and the ability to maintain mitotic arrest.

Conclusions:

Mammalian cells globally stabilize their transcriptome during prolonged mitotic arrest.
Mitotic mRNA stabilization is a critical adaptation for cell viability, buffering mRNA levels in the absence of transcription.
PABPC1&4 plays a vital role in maintaining mitotic mRNA stability and supporting prolonged mitotic arrest.