IGF2 has been shown to be expressed preferentially from the paternally
derived allele, although the maternal allele can be found active duri
ng both prenatal and postnatal development as well as in neoplastic tu
mours in humans. We addressed here whether or not the biallelic expres
sion patterns that can be seen during postnatal human liver developmen
t reflected a coordinated change in the activities of the four promote
rs of human IGF2. We show here that the P2, P3 and P4 promoters, but n
ot the P1 promoter, display monoallelic activity in embryonic, neonata
l and younger infant liver specimens. The P2, P3 and P4 promoters can,
however, be found active either monoallelically or biallelically or e
ven monoallelically on opposite parental alleles in older infant and a
dult liver specimens. In contrast, H19, which is closely linked to IGF
2, is monoallelically expressed in all postnatal liver samples analyse
d. We conclude that the functional imprinting status of IGF2 during po
stnatal liver development appears to be promoter/enhancer-specific and
either partly or completely independent of H19.