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

• Published in: Journal of experimental botany Vol. 68; no. 21/22; pp. 5787 - 5800
• Main Authors: Sang, Sihong, Chen, Yao, Yang, Qiaofeng, Wang, Peng
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 16-12-2017
• Subjects: Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Carrier Proteins - genetics; Carrier Proteins - metabolism; Chromatin - metabolism; Chromatin Immunoprecipitation; Flowers - genetics; Flowers - growth & development; Gene Silencing; Growth and Development; Histone Deacetylases - genetics; Histone Deacetylases - metabolism; MADS Domain Proteins - genetics; MADS Domain Proteins - metabolism; Phosphotransferases (Alcohol Group Acceptor) - genetics; Phosphotransferases (Alcohol Group Acceptor) - metabolism; Research Papers; Transcriptional Activation; AtIPK2β; FLC expression; chromatin silencing; FVE; Arabidopsis; flowering time; transcriptional regulation
• DOI: 10.1093/jxb/erx397
• EISSN: 1460-2431
• ISSN: 0022-0957

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.