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

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 defectivel (*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. DEDI 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.

Dawei Dai, Janaki S. Mudunkothge, Mary Galli, Si Nian Char, Ruth Davenport, Xiaojin Zhou, Jeffery L. Gustin, Gertraud Spielbauer, Junya Zhang, W. Brad Barbazuk, Bing Yang, Andrea Gallavotti, A. Mark Settles