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

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 and A. Mark Settles ()
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Dawei Dai: University of Florida
Janaki S. Mudunkothge: University of Florida
Mary Galli: Waksman Institute, Rutgers University
Si Nian Char: Bond Life Sciences Center, University of Missouri
Ruth Davenport: University of Florida
Xiaojin Zhou: Chinese Academy of Agricultural Sciences
Jeffery L. Gustin: University of Florida
Gertraud Spielbauer: University of Florida
Junya Zhang: University of Florida
W. Brad Barbazuk: University of Florida
Bing Yang: Bond Life Sciences Center, University of Missouri
Andrea Gallavotti: Waksman Institute, Rutgers University
A. Mark Settles: University of Florida

Nature Communications, 2022, vol. 13, issue 1, 1-11

Abstract: Abstract 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.

Date: 2022
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DOI: 10.1038/s41467-022-33055-9

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