[~ ERSPECTIVES endosperm has a paternal excess (2m: 2p) and undergoes greater mitotic activity than control endosperms (2m: lp, 4m: 2p). When the diploid is the pollen parent, the endosperm has a maternal excess (4m: lp), mitotic activity is reduced and maternal tissue remains unconsumed within the kernel9. Similar reciprocal differences in interploidy crosses have been reported from a wide of future offspring. A good example would be a gene for a placental growth factor. A new mutant allele that causes increased nutrient demands on the mother, but only when the allele is paternally derived, has a selective advantage over an established nonimprinted allele because the imprinted allele acquires extra nutrients for its own embryo at the expense of maternal halftaxonomic range of angiosperms 10. Analogous data come from the experimental manipulation of mouse development and clinical observations of humans. The extraembryonic membranes of gynogenetic and parthenogenetic mouse embryos (2m: 0p) develop poorly, but early development of the embryo itself is more or less normal. Androgenetic mouse embryos (0m: 2p), in contrast, undergo little embryonic development but have welldeveloped membranes. Both types of embryos abort~. Similarly, human triploid foetuses develop a large placenta if the extra genome is paternal, but have little placental tissue if the extra genome is maternal 12. Several chromosome deletions in humans and uniparental disomies in mice indicate that the expression of some genes in these regions depends on parental origin. The most striking example in humans is deletion of 15q11-13. Maternal loss of this seg-lm: lp 2m: 2p 3m: 2p 2m: lp 4m: 2p 5m: 2p

3. m. l.. p. 6m2p 4m: lp