Huge thanks to @claudiakohler11.bsky.social for her unwavering support of my work, and a special shout-out to Ushi, as well as to Varsha and Sofia—my fantastic former MSc students—for their invaluable contributions to this project! A dream team!

Our data support a model in which a primary siRNA trigger arises in the maternal integuments of the cer7 seed coat, reaches the embryo, and drives PTGS amplification, leading to seed abortion.

We also found that ectopic siRNAs in cer7 compete with key miRNAs for AGO1 loading, and together with PTGS of embryogenesis-related genes, lead to embryo arrest.

Consistent with a sporophytic maternal effect, expressing CER7 in the seed coat suppresses seed abortion, demonstrating a maternal control of embryo development via an RNA decay safeguard pathway in the sporophytic maternal plant.

Our genetic analysis further reveals that the PTGS trigger originates in the maternal sporophyte and is amplified in the fertilization products, ultimately causing seed abortion.

Embryo arrest in cer7 mutants is suppressed in rdr6 background, showing that the defect is linked to ectopic post-transcriptional gene silencing (PTGS).

We found that mutations on core subunit of the RNA-processing exosome RRP45B (CER7) induces early embryo arrest dependent on the sporophytic maternal plant genotype.