# Molecular mechanisms reprogramming transcription in quiescent cells

> **NIH NIH P20** · UNIVERSITY OF NORTH DAKOTA · 2022 · $182,367

## Abstract

The long-term goal of the proposed research is to characterize the molecular mechanism(s) by which cells 
are reprogrammed into quiescence. This reprogramming is essential for cells to maintain viability over 
long periods of time without divisions, such as quiescent stem cells and memory lymphocytes. On the 
other hand, this reprogramming also allows early-disseminated cancer cells to evade treatment by 
maintaining their state of quiescence. Therefore, deciphering the mechanisms and factors involved in 
cellular quiescence is both a fundamental biological question and informative in health and disease. 
We are approaching this in a systematic manner by focusing on a model organism, the fission yeast S. 
pombe. This model has a ‘minimal set’ of genes allowing viable long-term quiescence, and retained 
epigenetic mechanisms such as histone marks and RNA interference, which are essential in non-dividing 
cells. By identifying this minimal set and using high-throughput approaches available in fission yeast, our 
goal is to understand the basic principles and key components of reprogramming in quiescence, without 
the confounding effects due to the added complexity of multicellular organisms, where differentiation and 
intercellular communication occur and affect quiescence. 
Among several pathways that we have found to be essential for quiescence maintenance, we are 
focusing specifically on two complementary factors, which are not only conserved across eukaryotes, but 
also most likely to impact our understanding of reprogramming: in aim 1, we will study how a core 
component of the Mediator complex is essential specifically in quiescent cells to maintain basal 
transcriptional activity; in aim 2, we will focus on ERH, a small enigmatic protein, which acts as a 
repressor of transcription in quiescence. We will employ a combination of genetic, genomic, biochemistry 
and bioinformatics approaches to understand how these two complementary regulators shape gene 
expression in quiescent cells. Because both Mediator and ERH are mis-expressed in cancers with strong 
metastatic potential, we expect our results to shed some light not only on transcriptional reprogramming in 
physiological quiescent cells, but also on how this process is mis-regulated in tumor dormancy.

## Key facts

- **NIH application ID:** 10895178
- **Project number:** 5P20GM104360-09
- **Recipient organization:** UNIVERSITY OF NORTH DAKOTA
- **Principal Investigator:** Benjamin Roche
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $182,367
- **Award type:** 5
- **Project period:** 2022-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10895178

## Citation

> US National Institutes of Health, RePORTER application 10895178, Molecular mechanisms reprogramming transcription in quiescent cells (5P20GM104360-09). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10895178. Licensed CC0.

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