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Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize
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Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize
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Journal Article
Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize
2022
Overview
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.
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
