Non-canonical role of a PHOSPHATE1 HOMOLOG 2 in suppressing seedling photomorphogenesis via the TOC1–PIF4 module

Photomorphogenesis, the light-driven development of seedlings, is governed by a complex network of transcription factors and circadian regulators. While the TIMING OF CAB EXPRESSION 1 (TOC1) is known to link circadian rhythms with light-responsive growth, the mechanisms fine-tuning its activity remain poorly understood. Here, we identify PHOSPHATE 1 HOMOLOG 2 (PHO1;H2) as a novel negative regulator of seedling photomorphogenesis in Arabidopsis . Loss-of-function pho1;h2 mutants exhibit hypersensitivity to light, characterized by markedly shorter hypocotyls and increased photopigment accumulation, whereas overexpression lines display reduced photomorphogenic response. We demonstrate that the N-terminal SPX domain of PHO1;H2 is both necessary and sufficient to repress seedling photomorphogenic growth. Mechanistically, in vitro and in vivo interaction assays reveal that the SPX domain physically binds and sequesters TOC1, inhibiting its regulatory function. This PHO1;H2-mediated sequestration of TOC1 alleviates the repression of PHYTOCHROME INTERACTING FACTOR 4 (PIF4), thereby promoting the expression of downstream genes involved in cell elongation and hormone signaling. Collectively, our findings reveal a competitive binding mechanism by which PHO1;H2 modulates the TOC1–PIF4 signaling axis, providing a crucial checkpoint for seedling growth in dynamic light environments.