First published online June 14, 2004
Development 131, 1303e (2004)
© The Company of Biologists Limited
Signalling RED for terminal differentiation
Gata1, a zinc-finger transcription factor, is essential for mammalian
erythropoiesis. Erythroid cells that lack Gata1 apoptose, while Gata1
overexpression blocks differentiation. However, Gata1-overexpressing erythroid
cells differentiate normally in vivo when wild-type cells are present,
indicating that these cells produce a red cell differentiation signal (REDS)
that rescues the defect in Gata1-overexpressing cells. On
p. 3183,
Gutiérrez et al. report that REDS is produced by committed erythroid
cells. The researchers combine a tissue-specific Cre/loxP system and
X inactivation to produce mice in which half the erythroid cells overexpress
Gata1 and half are Gata1 null. These embryos are anaemic and
die by E14, supporting a homotypic signalling mechanism in which mature
erythroid cells produce REDS. Importantly, these results indicate that
terminal differentiation during erythropoiesis (and presumably during other
differentiation programmes) is not achieved by simply turning off self-renewal
signals, but also requires specific differentiation signals.
Related articles in Development:
- Homotypic signalling regulates Gata1 activity in the erythroblastic island
- Laura Gutiérrez, Fokke Lindeboom, An Langeveld, Frank Grosveld, Sjaak Philipsen, and David Whyatt
Development 2004 131: 3183-3193.
[Abstract]
[Full Text]
