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First published online September 9, 2004
In this issue |
The co-factor iron is essential for life but its organismal level must be tightly controlled to prevent severe consequences, ranging from anaemia (when too little iron is present) to iron-induced tissue damage (when too much is present). The iron transporter ferroportin 1 (Fpn1) is central to iron homeostasis. On p. 4871, Mok and co-workers describe how Fpn1 dysregulation interferes with spleen organogenesis in polycythaemia (Pcm) mutant mice. In these mice, an Fpn1 promoter mutation causes Fpn1 upregulation and iron overload during early postnatal development. The researchers show that embryonic Fpn1 mRNA and protein expression are both downregulated in Pcm mutant placenta and liver. However, in the embryonic spleen, although Fpn1 mRNA expression is downregulated, protein expression is upregulated, presumably through post-transcriptional regulation. Consequently, iron efflux from the spleen is increased, causing iron deficiency and stromal cell death, and, ultimately, red and white pulp defects. Thus, suggest the researchers, the Pcm mutant mouse provides a new model in which to study spleen organogenesis.
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