ELF6 mutation suppresses the dwarf phenotype of Arabidopsis ino80 mutant by modulating cell cycle progression.

The chromatin-remodeling factor INO80 is conserved across eukaryotes and plays important roles in various biological processes. However, its upstream regulators remain unclear. This study aimed to identify new regulators of INO80 in Arabidopsis and to uncover its molecular mechanism in plant growth. EMS mutagenesis screening was performed to find suppressors of the Arabidopsis ino80-5 mutant. RNA-seq identified key target genes, which were validated through cellular phenotypic analysis. ChIP-seq and ChIP-qPCR assays were performed to examine the chromatin binding levels of H2A.Z, INO80, and ELF6. Loss of INO80 delays plant development, increases cell cycle gene expression, and reduces cell size and ploidy, all of which are reversed by the G126E mutation in ELF6. INO80 and ELF6 are required for maintaining H2A.Z but not H3K27me3 levels. Both proteins bind similar DNA regions; however, the stabilizing G126E mutation in ELF6 disrupts INO80 binding at the transcription start sites of cell cycle genes. These findings show that the G126E missense mutation in ELF6 rescues the growth defect of the ino80-5 mutant, indicating that ELF6 acts as an upstream regulator of INO80 in plant growth. Moreover, the data support that ELF6 competes with INO80 for chromatin binding to precisely regulate gene expression during the plant cell cycle.