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Updated: Jun 7, 2026

In vivo Application of the REMOTE-control System for the Manipulation of Endogenous Gene Expression
Published on: March 29, 2019
Oct1 is a switchable, bipotential stabilizer of repressed and inducible transcriptional states
Arvind Shakya1, Jinsuk Kang, Jeffrey Chumley
1Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA.
Abstract:
Little is known regarding how the Oct1 transcription factor regulates target gene expression. Using murine fibroblasts and two target genes, Polr2a and Ahcy, we show that Oct1 recruits the Jmjd1a/KDM3A lysine demethylase to catalyze the removal of the inhibitory histone H3K9 dimethyl mark and block repression. Using purified murine T cells and the Il2 target locus, and a colon cancer cell line and the Cdx2 target locus, we show that Oct1 recruits the NuRD chromatin-remodeling complex to promote a repressed state, but in a regulated manner can switch to a different capacity and mediate Jmjd1a recruitment to block repression. These findings indicate that Oct1 maintains repression through a mechanism involving NuRD and maintains poised gene expression states through an antirepression mechanism involving Jmjd1a. We propose that, rather than acting as a primary trigger of gene activation or repression, Oct1 is a switchable stabilizer of repressed and inducible states.
Insights
The Oct1 transcription factor acts as a switchable stabilizer, recruiting NuRD for repression or Jmjd1a to block repression and maintain poised gene expression states.
Area of Science:
- Molecular Biology
- Gene Regulation
- Epigenetics
Background:
- The precise mechanisms by which Oct1 transcription factor regulates target gene expression remain largely unknown.
- Understanding Oct1's role is crucial for deciphering gene expression control.
Purpose of the Study:
- To elucidate how Oct1 influences gene expression by recruiting specific protein complexes.
- To investigate Oct1's dual role in maintaining repressed and inducible gene states.
Main Methods:
- Utilized murine fibroblasts, purified murine T cells, and a colon cancer cell line.
- Analyzed target gene loci including Polr2a, Ahcy, Il2, and Cdx2.
- Investigated the recruitment of Jmjd1a/KDM3A and the NuRD complex.
Main Results:
- Oct1 recruits Jmjd1a/KDM3A to remove H3K9 dimethyl marks, blocking repression of Polr2a and Ahcy.
- Oct1 recruits the NuRD complex to establish a repressed state at the Il2 and Cdx2 loci.
- Oct1 can switch its function, recruiting Jmjd1a to block repression in a regulated manner.
Conclusions:
- Oct1 acts as a switchable stabilizer, maintaining repressed states via NuRD and poised states via Jmjd1a.
- Oct1 does not primarily trigger activation or repression but stabilizes existing states.
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