Cell cycle progression during endosperm development in Zea mays depends on parental dosage effects.

Interploidy crosses in flowering plants often cause seed abortion. Studies in maize have shown that failure of kernel development results from dosage effects among products of imprinted but as-yet-unknown genes in the endosperm, and that the operative stoichiometry is established for a ratio of two maternal genomes to one paternal genome. In this study, we used flow cytometry to monitor cell cycle activities in developing endosperms obtained after reciprocal crosses between diploid and tetraploid maize individuals. Our data show that dosage effects alter critical events involved in the establishment of endoreduplication during maize endosperm development. Particularly, maternal genomic excess (4x x 2x crosses) forces endosperm cells to enter early into endoreduplication while paternal genomic excess (2x x 4x crosses) prevents its establishment. Our results also suggest that altering mechanisms depend on two different sets of cell cycle regulatory genes--one imprinted through the female that is required for mitotic arrest, and another responsible for re-entry into S phase that is imprinted through the male. Further, molecular and physiological analyses should provide insights into the interaction of parental imprinting action and cell cycle regulation during endosperm development.