Prolonged expression of a putative invertase inhibitor in micropylar endosperm suppressed embryo growth in arabidopsis

Abstract

Proper seed development requires coordinated growth among the three genetically distinct components, the embryo, the endosperm, and the seed coat. In Arabidopsis, embryo growth rate accelerates after endosperm cellularization, which requires a chromatin-remodeling complex, the FIS2-Polycomb Repressive Complex 2 (PRC2). After cellularization, the endosperm ceases to grow and is eventually absorbed by the embryo. This sequential growth pattern displayed by the endosperm and the embryo suggests a possibility that the supply of sugar might be shifted from the endosperm to the embryo upon endosperm cellularization. Since invertases and invertase inhibitors play an important role in sugar partition, we investigated their expression pattern during early stages of seed development in Arabidopsis. Two putative invertase inhibitors (InvINH1 and InvINH2) were identified as being preferentially expressed in the micropylar endosperm that surrounds the embryo. After endosperm cellularization, InvINH1 and InvINH2 were down-regulated in a FIS2-dependent manner. We hypothesized that FIS2-PRC2 complex either directly or indirectly represses InvINH1 and InvINH2 to increase invertase activity around the embryo, making more hexose available to support the accelerated embryo growth after endosperm cellularization. In support of our hypothesis, embryo growth was delayed in transgenic lines that ectopically expressed InvINH1 in the cellularized endosperm. Our data suggested a novel mechanism for the FIS2-PRC2 complex to control embryo growth rate via the regulation of invertase activity in the endosperm.