22Seed development is sensitive to parental dosage, with excess maternal or paternal 23 genomes creating reciprocal phenotypes. Paternal genomic excess results in extensive 24 endosperm proliferation without cellularization and eventual seed abortion. We 25 previously showed that loss of the RNA POL IV gene nrpd1 in tetraploid fathers 26 represses seed abortion in paternal excess crosses. Here we show genetically that 27 RNA-directed DNA methylation (RdDM) pathway activity in the paternal parent is 28 sufficient to determine the viability of paternal excess seeds. The status of the RdDM 29 pathway in paternal excess endosperm does not impact seed viability. Comparison of 30 endosperm transcriptomes, DNA methylation, and small RNAs from balanced and 31 paternal excess endosperm demonstrates that paternal excess seed abortion is unlikely 32 to be dependent on either transposable element or imprinted gene mis-regulation. We 33 suggest instead that loss of paternal RdDM modulates expression at a small subset of 34 genes and desensitizes endosperm to paternal excess. Finally, using allele-specific 35 transcription data, we present evidence of a transcriptional buffering system that up-36
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