ALFIN-LIKE Proteins Orchestrate H3K4me3-H3K27me3 Crosstalk to Regulate Plant Embryogenesis
In multicellular organisms such as animals and plants, development requires the precise regulation of gene expression, mediated not only by transcription factors but also by chromatin-based mechanisms. Among these, histone modifications like H3K4me3 and H3K27me3 play opposing roles in gene activation and repression, respectively. In Arabidopsis thaliana, H3K27me3 is deposited by the Polycomb Repressive Complex 2 (PRC2), while Trithorax group (TrxG) proteins mediate H3K4me3 deposition. While the functions of these writer complexes have been extensively studied, far less is known about the histone mark readers that interpret these modifications during development. Here, we investigate the antagonistic interplay between H3K27me3 and H3K4me3 during Arabidopsis embryogenesis. We identify a developmentally specific interaction between the FIS-PRC2 complex and ALFIN-LIKE (AL) proteins--a family of plant-specific PHD domain proteins that read H3K4me3. Our findings reveal a dynamic competition between these two marks during early embryogenesis that helps shape the epigenomic landscape of the developing seed. Disruption of AL function leads to severe developmental defects and loss of cell identity in early embryos. Moreover, loss of ALs impairs H3K4me3 deposition, resulting in aberrant spreading of H3K27me3, misregulation of developmental genes, and defects that persist into adult plant traits. Together, our results show that proper embryonic development relies on a finely tuned antagonism between activating and repressive chromatin states--an interplay orchestrated not only by their writers but also by specific readers that translate these epigenetic cues into developmental outcomes.