Journal
JOURNAL OF IMMUNOLOGY
Volume 178, Issue 5, Pages 3038-3047Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.5.3038
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Funding
- NCI NIH HHS [CA 009560] Funding Source: Medline
- NCRR NIH HHS [K26 RR026099] Funding Source: Medline
- NIGMS NIH HHS [GM 008152] Funding Source: Medline
- NIH HHS [K26 OD010945] Funding Source: Medline
- NINDS NIH HHS [NS 046468, K02 NS046468, R01 NS040748, NS 040748] Funding Source: Medline
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Early growth response (Egr) proteins comprise a family of transcriptional regulators (Egrl-4) that modulate gene expression involved in the growth and differentiation of many cell types. In particular, Egr1 is widely believed to have an essential role in regulating monocyte/macrophage differentiation. However, Egr1-deficient mice have normal numbers of functional macrophages, an observation that has led to the hypothesis that other Egr proteins may compensate for Egr1 function in vivo. We examined whether other Egr transcription factors have a functionally redundant role in monocyte/macrophage differentiation. Egr1 and Egr3 expression was found to be induced in myeloid cells when they were differentiated into macrophages by treatment with M-CSF, whereas Egr2 was minimally induced and Egr4 was not detected. In either Egr1/Egr3 or Egrl/ Egr2 double homozygous mutant mice, macrophage differentiation and function remained unimpaired. Additionally, the expression of molecules that broadly inhibit Egr function failed to block commitment to the monocytic lineage or inhibit the maturation of monocyte precursors. Finally, several hemopoietic growth factors were found to induce Egr gene expression, indicating that Egr gene expression is not cell lineage specific. Taken together, these results demonstrate that Egr transcription factors are neither essential for nor specific to monocyte/macrophage differentiation.
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