Arabidopsis inositol polyphosphate multikinase delays flowering time through mediating transcriptional activation of FLOWERING LOCUS C

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 (AtIPK2 beta) functions in flowering time control by mediating transcriptional regulation of FLC at the chromatin level. The atipk2 beta mutant flowers earlier, and AtIPK2 beta overexpressing plants exhibit late-flowering phenotypes. Quantitative reverse transcription-PCR (qRT-PCR) revealed that AtIPK2 beta promotes FLC expression. We performed chromatin immunoprecipitation-qPCR (ChIP-qPCR) assays and found that AtIPK2 beta binds to FLC chromatin. Further analysis showed that AtIPK2 beta interacts with FVE, a key repressor required for epigenetic silencing of FLC. qRT-PCR, ChIP-qPCR, and genetic analysis demonstrated that AtIPK2 beta is involved in FVE-mediated transcriptional regulation of FLC by repressing the accumulation of FVE on FLC. Moreover, we found that AtIPK2 beta 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 AtIPK2 beta negatively regulates flowering time by blocking chromatin silencing of FLC.