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Updated: May 31, 2026

Mouse Fetal Liver Culture System to Dissect Target Gene Functions at the Early and Late Stages of Terminal Erythropoiesis

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Dissecting polycomb complexes for enhanced fetal hemoglobin production.

Paul Kaminski¹, Kristen Min², Elizabeth A Traxler³

¹University of Pennsylvania, Philadelphia, Pennsylvania, United States.

|May 29, 2026

Summary

This summary is machine-generated.

Targeting Polycomb Repressive Complex (PRC) components selectively can reactivate fetal hemoglobin (HbF). A modified EZH2 subunit (EZH2D14) shows promise for treating hemoglobinopathies like sickle cell disease.

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Area of Science:

Epigenetics and Gene Regulation
Hematology
Molecular Biology

Background:

Polycomb repressive complexes (PRC1 and PRC2) are crucial regulators of gene expression during development.
Reversing the fetal-to-adult hemoglobin switch is a therapeutic target for sickle cell disease and b-thalassemia.
Current PRC inhibitors have limited use due to broad cellular effects.

Purpose of the Study:

To investigate selective perturbations of PRC components for targeted fetal hemoglobin (HbF) reactivation.
To assess if HbF can be reactivated without complete loss of PRC function.
To identify specific PRC modifications with therapeutic potential.

Main Methods:

High-density CRISPR-Cas9 mutagenesis screen on PRC components.
Generation and characterization of a modified EZH2 subunit (EZH2D14) lacking part of the CXC domain.
Functional assays in erythroid cells and a mouse model of hemoglobin switching.

Main Results:

A CRISPR screen identified EZH2 exon 14 skipping (EZH2D14) as a key modification.
EZH2D14 selectively relieves HbF repression while maintaining cellular fitness.
EZH2D14 retains H3K27 methylation and repression of a subset of PRC target genes.
The identified pathway for EZH2 control of HbF functions in a relevant mouse model.

Conclusions:

Partial disruption of PRC components, specifically targeting non-enzymatic domains, can yield selective phenotypes.
EZH2D14 demonstrates therapeutic potential for reactivating HbF in hemoglobinopathies.
Selective targeting of chromatin-modifying complexes offers a promising therapeutic strategy.