TIE1 acts as a maternal brake on fertilization-independent endosperm development by associating with PRC2 to enforce imprinting

Abstract

Fully autonomous apomixis with fertilization-independent embryo and endosperm development enables the production of clonal seeds to fix crop hybrid vigour. However, the mechanisms underlying autonomous endosperm development remain unclear. Here we show that TIE1 acts as a maternally expressed transcriptional repressor inhibiting autonomous endosperm. The disruption of four TIEs in tie1 tie2 tie3 tie4 (tieQ) mutants triggers the development of autonomous endosperm, recapitulating the phenotypes observed in fertilization-independent seeds (fis)-class mutants. TIE1 exhibits maternal genomic imprinting similar to MEDEA (MEA) that encodes a core component of the FIS–POLYCOMB REPRESSIVE COMPLEX 2 (PRC2). TIE1 recruits FIS–PRC2 to transcriptionally silence a subset of its target genes whose activation would otherwise trigger endosperm development in the absence of fertilization. Our findings reveal a maternally controlled brake mechanism that prevents autonomous endosperm development, providing both a molecular framework for understanding apomictic seed formation and a possible tool for engineering synthetic apomixis to fix heterosis in crops. Plants that form seeds without fertilization could fix hybrid vigour. This study determines that the maternal protein TIE1 serves as a brake to prevent autonomous seed development without fertilization.