Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize

Xenia effects describe the genetic contribution of pollen to seed phenotypes. Here the authors show that paternal imprinting of Ded1 contributes to the xenia effect in maize by setting the pace of endosperm development. Historically, xenia effects were hypothesized to be unique genetic contributions of pollen to seed phenotype, but most examples represent standard complementation of Mendelian traits. We identified the imprinted dosage-effect defective1 (ded1) locus in maize (Zea mays) as a paternal regulator of seed size and development. Hypomorphic alleles show a 5-10% seed weight reduction when ded1 is transmitted through the male, while homozygous mutants are defective with a 70-90% seed weight reduction. Ded1 encodes an R2R3-MYB transcription factor expressed specifically during early endosperm development with paternal allele bias. DED1 directly activates early endosperm genes and endosperm adjacent to scutellum cell layer genes, while directly repressing late grain-fill genes. These results demonstrate xenia as originally defined: Imprinting of Ded1 causes the paternal allele to set the pace of endosperm development thereby influencing grain set and size.

Automated summary

The paternal imprinting of Ded1 in maize contributes to the xenia effect by regulating the pace of endosperm development. This study provides evidence for the existence of xenia effects and reveals the regulatory mechanism of endosperm development.