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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Intrinsic requirement for zinc finger transcription factor Gfi-1 in neutrophil differentiation.

We report essential roles of zinc finger transcription factor Gfi-1 in myeloid development. Gene-targeted Gfi-1(-/-) mice lack normal neutrophils and are highly susceptible to abscess formation by gram-positive bacteria. Arrested, morphologically atypical, Gr1(+)Mac1(+) myeloid cells expand with age in the bone marrow. RNAs encoding primary but not secondary or tertiary neutrophil (granulocyte) granule proteins are expressed. The atypical Gr1(+)Mac1(+) cell population shares characteristics of both the neutrophil and macrophage lineages and exhibits phagocytosis and respiratory burst activity. Reexpression of Gfi-1 in sorted Gfi-1(-/-) progenitors ex vivo rescues neutrophil differentiation in response to G-CSF. Thus, Gfi-1 not only promotes differentiation of neutrophils but also antagonizes traits of the alternate monocyte/macrophage program.[1]

References

  1. Intrinsic requirement for zinc finger transcription factor Gfi-1 in neutrophil differentiation. Hock, H., Hamblen, M.J., Rooke, H.M., Traver, D., Bronson, R.T., Cameron, S., Orkin, S.H. Immunity (2003) [Pubmed]
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