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Related Experiment Video

Updated: Jan 23, 2026

Studying the Protein Quality Control System of D. discoideum Using Temperature-controlled Live Cell Imaging

Studying the Protein Quality Control System of D. discoideum Using Temperature-controlled Live Cell Imaging

Published on: December 2, 2016

Protein quality control meets transcriptome remodeling under stress.

Veena Mathew¹, Peter C Stirling¹

¹Terry Fox Laboratory, British Columbia Cancer Agency. 675 West 10th Avenue, Vancouver, British Columbia, V5Z1L3, Canada.

|June 22, 2019

Summary

Cells suppress ribosome production during genotoxic stress by sequestering the splicing factor Hsh155 into nuclear aggregates. This process, regulated by TORC1, promotes intron retention and aids stress recovery.

Keywords:

Saccharomyces cerevisiae genotoxic stress protein aggregate ribosome production splicing

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Area of Science:

Cellular stress response
Molecular biology
Genetics

Background:

Genotoxic stress necessitates cellular coordination, including cell cycle arrest, DNA repair, and proteome remodeling.
Ribosome production suppression is a key stress response in yeast, primarily studied at the transcriptional level.

Purpose of the Study:

To investigate the post-transcriptional mechanisms regulating ribosome production during genotoxic stress.
To elucidate the dynamic behavior of the splicing factor Hsh155 in response to cellular stress.

Main Methods:

Analysis of Hsh155 dynamics and localization within the nucleus.
Investigating the role of Hsh155 sequestration in protein aggregates.
Assessing the impact of Hsh155 relocalization on intron retention in ribosomal protein genes.

Main Results:

Hsh155, a component of the SF3B complex (homologous to human SF3B1), disassembles from its complex during stress.
Disassembled Hsh155 is sequestered into nuclear protein aggregates, suppressing ribosome biogenesis post-transcriptionally.
This sequestration promotes intron retention in ribosomal protein gene transcripts.

Conclusions:

Hsh155 sequestration is a critical post-transcriptional mechanism for suppressing ribosome production under genotoxic stress.
TORC1 signaling and molecular chaperones facilitate Hsh155 relocalization, contributing to stress tolerance and recovery.