# Understanding mRNA Condensation and Its Role in Translational Control during Stress

> **NIH NIH F30** · UNIVERSITY OF CHICAGO · 2023 · $52,694

## Abstract

Project Summary/ Abstract
 How cells dynamically control their proteome in response to stress is a fundamental aspect of
understanding how organisms are able to react to changing environments. Two representative features of the
cellular stress response, which is universally conserved across eukarya and occurs in response to a variety of
different noxious environmental conditions, are 1) the upregulation of the cytoprotective heat shock proteins
and 2) biomolecular condensation of RNA and protein into assemblies. Most translation is shut down, while
proteins involved in the stress response are efficiently produced. How translation is reprogrammed to favor
heat shock protein production post-transcriptionally is poorly understood, but biomolecular condensation has
been linked to translational control. Basic questions are incompletely answered: 1) Which mRNAs condense in
response to stress? 2) What cellular mechanisms are responsible for mRNA condensation? And 3) What is the
functional relevance of mRNA condensation to translational control?
 Herein, we present unpublished work measuring mRNA solubility of >5,000 genes during temperature
stress in S. cerevisiae by biochemical sedimentation followed by RNA-Sequencing. These data inform our
hypothesis that blocking translation initiation triggers condensation of an mRNA through specific binding by
unknown protein factor(s). We also predict that mRNA condensation during stress is an adaptive process
contributing to the preferential translation of stress response messages. To test these hypotheses, we aim to
confirm that blocking translation initiation triggers mRNA condensation both on a transcriptome-wide and
individual message level, to determine protein factors required for mRNA condensation, and to test the role of
mRNA condensation in translational reprogramming during stress. Preliminary data measuring the solubility of
both native and reporter mRNAs support that blocking translation initiation triggers condensation. We have
identified and will interrogate a set of the translation initiation factors as candidates putatively required for
mRNA condensation. We will test whether the candidates are required for mRNA condensation and measure
the translational effect of perturbing mRNA condensation during stress.
 Biomolecular condensates are intimately related to cellular RNA homeostasis, and their dysfunction has
been linked to the pathogenesis of several neurodegenerative diseases including Alzheimer's and Parkinson's.
Knowledge of how mRNAs condense and the functional role of condensation informs disease pathogenesis
and may inform future treatments for those affected.

## Key facts

- **NIH application ID:** 10614516
- **Project number:** 5F30ES032665-03
- **Recipient organization:** UNIVERSITY OF CHICAGO
- **Principal Investigator:** Hendrik Glauninger
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $52,694
- **Award type:** 5
- **Project period:** 2021-04-01 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10614516

## Citation

> US National Institutes of Health, RePORTER application 10614516, Understanding mRNA Condensation and Its Role in Translational Control during Stress (5F30ES032665-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10614516. Licensed CC0.

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