The plant hormone auxin controls many aspects of plant growth and development by promoting the degradation of Auxin/Indole-3-acetic acid (Aux/IAA) proteins. The domain II (DII) of Aux/IAA proteins is sufficient for eliciting the degradation by directly interacting with the auxin receptor F-box protein TIR1 to form a TIR1/AFBs-Aux/IAA complex in an auxin-dependent manner. However, the underlying mechanisms of fine-tuning Aux/IAA degradation by auxin stimuli remain to be elucidated. Here, we show that OsIPK2, a rice (Oryza sativa) inositol polyphosphate kinase, directly interacts with an Aux/IAA protein OsIAA11 to repress its degradation. In a rice protoplast transient expression system, the auxin-induced degradation of Myc-OsIAA11 fusion was delayed by co-expressed GFP-OsIPK2 proteins. Furthermore, expressing additional OsIPK2 or its N-terminal amino acid sequence enhanced the accumulation of OsIAA11 proteins in transgenic plants, which in turn caused defects in lateral root formation and auxin response. Taken together, we identify a novel co-factor of Aux/IAA in auxin signaling and demonstrate its role in regulating lateral root development.

Phosphorus (P) is one kind of growth-limiting nutrient for plants, which is taken up by root tissue from the environment as inorganic phosphate (P_i). To maintain an appropriate status of cellular P_i, plants have developed sophisticated strategies to sense P_i level and modulate their root system architecture (RSA) under the ever-changing growth condition. However, the molecular basis underlying the mechanism remains elusive. Inositol polyphosphate kinase (IPK2) is a key enzyme in the inositol phosphate metabolism pathway, which catalyzes the phosphorylation of IP₃ into IP₅ by consuming ATP. In this study, the function of a rice inositol polyphosphate kinase gene (OsIPK2) in plant P_i homeostasis and thus physiological response to P_i signal were characterized. As a biosynthetic gene for phytic acid in rice, overexpression of OsIPK2 led to distinct changes of inositol polyphosphate profiles and an excessive accumulation of P_i level in transgenic rice under P_i-sufficient conditions. The inhibitory effects of OsIPK2 on root growth were alleviated by P_i-deficient treatment compared with wild-type plants, suggesting the involvement of OsIPK2 in the P_i-regulated reconstruction of RSA. In OsIPK2-overexpressing plants, the altered acid phosphatase (APases) activities and misregulation of P_i starvation induced (PSI) genes were observed in roots under different P_i supply conditions. Notably, the expression of OsIPK2 also altered the P_i homeostasis and root system architecture in transgenic Arabidopsis. Taken together, our findings demonstrated that OsIPK2 plays an important role in P_i homeostasis and root system architecture adjustment in response to different environmental P_i levels in plant.

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.