In mice, the absence of the leucine zipper transcription factor p45NF-E2 results in thrombocytopenia (reduced platelet numbers), impaired placental vascularisation and intrauterine growth restriction (IUGR). It is generally assumed that the lack of embryonic platelets causes the growth problems seen in p45NF-E2-deficient embryos, but now, Berend Isermann and colleagues report that the placental defect and IUGR of p45NF-E2 null mouse embryos is unrelated to thrombocytopenia (see p. ). Instead, they show that p45NF-E2 is expressed in trophoblast cells where it is required for normal syncytiotrophoblast formation, placental vascularisation and embryonic growth. Expression of p45NF-E2 in labyrinthine trophoblast cells, they report, colocalises with the expression of Gcm1, a zinc-finger transcription factor crucial for syncytiotrophoblast formation. Finally, they show that p45NF-E2 cell-autonomously represses Gcm1-dependent syncytiotrophoblast formation by inhibiting acetylation in vitro and in vivo. The identification of this novel function for p45NF-E2 during placental development provides new insights into the mechanisms underlying IUGR, a poorly understood but common complication of human pregnancies.
