Timely flowering is critical for successful reproduction and seed yield in plants. A diverse range of regulators have been found to control flowering time in response to environmental and endogenous signals. Among these regulators, FLOWERING LOCUS C (FLC) acts as a central repressor of floral transition by blocking the expression of flowering integrator genes. Here, we report that Arabidopsis inositol polyphosphate multikinase (AtIPK2β) functions in flowering time control by mediating transcriptional regulation of FLC at the chromatin level. The atipk2β mutant flowers earlier, and AtIPK2β overexpressing plants exhibit late-flowering phenotypes. Quantitative reverse transcription-PCR (qRT-PCR) revealed that AtIPK2β promotes FLC expression. We performed chromatin immunoprecipitation-qPCR (ChIP-qPCR) assays and found that AtIPK2β binds to FLC chromatin. Further analysis showed that AtIPK2β interacts with FVE, a key repressor required for epigenetic silencing of FLC. qRT-PCR, ChIP-qPCR, and genetic analysis demonstrated that AtIPK2β is involved in FVE-mediated transcriptional regulation of FLC by repressing the accumulation of FVE on FLC. Moreover, we found that AtIPK2β associates with HDA6, an interaction partner of FVE mediating FLC chromatin silencing, and attenuates HDA6 accumulation at the FLC locus. Taken together, these findings suggest that AtIPK2β negatively regulates flowering time by blocking chromatin silencing of FLC.

Seed vigor is a key agronomic trait that integrates germination capacity and seedling establishment, critically influencing rice productivity. Inositol hexakisphosphate (IP₆) serves as a major phosphorus reservoir in seeds, yet its regulatory mechanism in seed vigor remains unclear. Here, we demonstrate that exogenous IP₆ application inhibited seed germination and seedling growth of japonica rice (Oryza sativa L. ssp. japonica cv. Zhonghua11) in a dose-dependent manner; 10 mM IP₆ reduced seed germination by 100%, while 100 μM IP₆ suppressed primary root length by 33.6% compared to the control. This inhibitory effect is likely mediated by antagonizing auxin signaling, as supported by suppressed DR5::GUS expression and altered transcription of auxin-responsive genes. OsIPK2, a key enzyme in IP₆ biosynthesis, showed high expression during early development in rice. RNA interference of OsIPK2 led to a 40.8–61.7% reduction in seed IP₆ content, 45.3–65% higher zinc (Zn) and iron (Fe) accumulation, and a 35.4–53.5% lower germination rate compared to wild-type (WT). Conversely, OsIPK2-RNAi seedlings exhibited enhanced growth and resistance to IP₆, which was associated with misregulation of auxin-responsive genes and a decrease in the repressive histone mark H3K27me3 at their loci. Furthermore, endogenous indole-3-acetic acid (IAA) levels significantly reduced in Ri-1 but unchanged in Ri-2, while abscisic acid (ABA) content and the IAA/ABA ratio remained unaltered compared to wild-type. Our findings reveal that OsIPK2 balances seed vigor and seedling development by modulating inositol phosphate metabolism, auxin responses, and epigenetic regulation, providing insights for improving seed quality in cereals. Whether the regulatory role of OsIPK2 in seed vigor is conserved across other rice subspecies requires further investigation.

Trichomes are specialized epidermal structures that play pivotal roles in plant defense against biotic and abiotic stresses. Inositol polyphosphate kinase 2 (IPK2) is a key enzyme in inositol phosphate metabolism with diverse functions in eukaryotic cellular processes. However, its involvement in trichome development remains uncharacterized. Here, we systematically analyzed the function of a rice inositol polyphosphate kinase gene (OsIPK2) in trichome development using transgenic rice lines and heterologously expressing Arabidopsis lines. Scanning electron microscopy (SEM) analysis revealed that OsIPK2 acts as an organ-specific modulator of trichome development in rice. Its overexpression repressed macrohair initiation and microhair elongation in leaves, while promoting trichome development on the glumes. Metabolomic profiling revealed that OsIPK2 overexpression reprogrammed cuticular wax metabolism in transgenic rice leaves, shifting fatty acid flux toward long-chain wax precursors and increasing soluble carbohydrate levels. Transcriptomic and qPCR analysis confirmed that OsIPK2 modulated the expression of genes involved in cuticular wax biosynthesis, auxin homeostasis, and the core trichome regulatory cascade in rice. Conversely, heterologous overexpression of OsIPK2 in Arabidopsis strongly suppressed trichome initiation and branching, resulting in drastically reduced trichome density and fewer trichome branches. These phenotypes were associated with the downregulation of the MYB-bHLH-WD40 (MBW) transcriptional complex and its downstream target genes. Collectively, our findings suggest that OsIPK2 modulated trichome development through organ- and species-specific mechanisms. In rice, it coordinated wax metabolism and the OsSPL10-OsSCR1/2-OsWOX3B-OsHL6 cascade to affect organ-specific trichome formation. In Arabidopsis, it inhibited trichome development by repressing the MBW complex. These results uncover a novel role of OsIPK2 in plant epidermal cell fate specification and advance our understanding of the molecular mechanisms underlying organ- and species-specific regulation of trichome development.