KIL transcription factors facilitate embryo growth in maize by promoting endosperm elimination via lytic cell death.

The endosperm is a transient nutritive tissue in plant seeds. During maize (Zea mays) grain development, 2 distinct endosperm cell death processes occur: in 1 process, the endosperm adjacent to the embryo scutellum (EAS) is completely dismantled; in the other, the starchy endosperm (SE) retains nutrient-packed cell corpses after grain filling. Here, we show that SE cell death degrades some organelles including the mitochondria and the endoplasmic reticulum, while preserving protein bodies, starch granules, and chromatin. In contrast, EAS cells undergo lytic cell death to remobilize stored nutrients through a complex corpse clearance process. Using single-cell transcriptome analysis, we identified 2 NAC transcription factors, KIRA-LIKE 1 (KIL1) and 2 (KIL2), as specifically upregulated in the EAS. Analyses using dominant and recessive loss-of-function kil mutants demonstrate that these genes redundantly promote cell death and corpse clearance in the EAS, but are not required for SE cell death. Reduced EAS cell death in kil loss-of-function mutants strongly impeded embryo growth, indicating that EAS elimination is crucial for optimal embryo development. Notably, kil1 and kil2 expression is regulated by DOSAGE-EFFECT DEFECTIVE1, an imprinted paternally expressed endosperm transcription factor. Our findings suggest paternal control over EAS cell death and the embryo-endosperm size ratio in maize, providing new leads to modulate this agronomically important trait.