Related Experiment Video
Updated: Aug 14, 2026

11:40
Retroviral Infection of Murine Embryonic Stem Cell Derived Embryoid Body Cells for Analysis of Hematopoietic Differentiation
Published on: October 20, 2014
PU.1 but not ets-2 is essential for macrophage development from embryonic stem cells
G W Henkel1, S R McKercher, H Yamamoto
1Burnham Institute, La Jolla Cancer Research Foundation, CA 92037, USA.
Blood
|October 15, 1996
Summary
The transcription factor PU.1 is crucial for macrophage development, as its absence in knockout cells blocked differentiation. In contrast, ets-2 knockout cells developed normally, highlighting PU.1's distinct role in blood cell lineage commitment.
Area of Science:
- Hematopoiesis and immunology
- Molecular biology and genetics
Background:
- Transcription factors regulate blood cell development.
- Lineage-restricted factors are key candidates for controlling hematopoietic cell differentiation.
Purpose of the Study:
- To compare the roles of transcription factors PU.1 and ets-2 in macrophage development.
- To investigate the necessity of PU.1 and ets-2 for hematopoietic stem cell differentiation into macrophages.
Main Methods:
- Generation of knockout embryonic stem (ES) cells lacking either the PU.1 or ets-2 gene.
- Assessment of macrophage differentiation potential in knockout ES cells using histochemical and immunohistochemical analyses.
- Detection of macrophage marker gene expression (c-fms, CD11b, CD18, and granulocyte-macrophage colony-stimulating factor receptor) via reverse transcriptase-polymerase chain reaction.
Main Results:
- Macrophage development was significantly impaired in PU.1 knockout ES cells.
- Key macrophage markers were undetectable in PU.1 knockout-derived cells.
- Macrophage development proceeded normally in ets-2 knockout ES cells.
Conclusions:
- The lineage-restricted transcription factor PU.1 plays a distinct and essential role in macrophage development.
- The ubiquitously expressed transcription factor ets-2 is not essential for macrophage development.
- These findings elucidate the specific regulatory mechanisms governing blood cell lineage commitment.

