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Related Experiment Video

Updated: Sep 15, 2025

High-throughput Purification of Affinity-tagged Recombinant Proteins

High-throughput Purification of Affinity-tagged Recombinant Proteins

Published on: August 26, 2012

Master transcription-factor binding sites constitute the core of early replication control elements.

Jesse L Turner^1,2, Laura Hinojosa-Gonzalez^3,4, Takayo Sasaki²

¹Department of Biological Science, Florida State University, Tallahassee, FL, 32306, USA.

The EMBO Journal

|July 17, 2025

Summary

Early Replication Control Elements (ERCEs) organize chromatin for early genome replication and transcription. These elements, composed of transcription factor binding sites (subERCEs), are crucial for cell fate transitions.

Keywords:

Cell Cycle Cell fate Transitions Genome Architecture Replication Timing Transcription

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Area of Science:

Genomics
Epigenetics
Molecular Biology

Background:

Eukaryotic genomes replicate according to a specific temporal order known as the replication timing (RT) program.
Replication timing is developmentally regulated and influences cell fate transitions, but the underlying mechanisms are not fully understood.

Purpose of the Study:

To elucidate the mechanisms controlling replication timing (RT).
To investigate the role of Early Replication Control Elements (ERCEs) in regulating RT, transcription, and chromatin architecture.

Main Methods:

Deletion analysis of cis-acting elements (ERCEs and subERCEs) in mouse embryonic stem cells (mESCs).
Assessment of effects on transcription and replication timing.
Analysis of transcription start sites.

Main Results:

Early Replication Control Elements (ERCEs) are compound elements, with their RT activity largely attributable to multiple transcription factor binding sites (subERCEs).
Deletion of subERCEs significantly impacted both transcription and replication timing.
Deletion of transcription start sites abolished transcription but only moderately affected replication timing.

Conclusions:

SubERCEs function as transcriptional enhancers that also structurally organize chromatin domains to promote early replication timing.
This mechanism may create a feed-forward loop, driving significant epigenomic changes during cell fate transitions.