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J EXP BOT:拟南芥开花时间的转录调控

已有 3806 次阅读 2017-11-19 15:06 |个人分类:每日摘要|系统分类:论文交流

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


First author: Sihong Sang; Affiliations: Wuhan University (武汉大学), Wuhan, China

Corresponding author: Sihong Sang


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 (成花转变) by blocking the expression of flowering integrator genes. Here, we report that Arabidopsis inositol polyphosphate multikinase (AtIPK2β; 多磷酸肌醇激酶) 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 (表观沉默) 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 (减弱) HDA6 accumulation at the FLC locus. Taken together, these findings suggest that AtIPK2β negatively regulates flowering time by blocking chromatin silencing of FLC.




适时的开花对于植物成功生殖和种子产量是至关重要的。有很多的调控子响应于环境和内源信号控制开花时间。在这些调控子中,FLC作为成花转变的中心抑制子,阻遏开花调控基因。本文报道了一个拟南芥多磷酸肌醇激酶AtIPK2β通过从染色质层面介导FLC的转录调控来控制开花时间。atipk2β突变体提前开花,而过表达AtIPK2β会延迟开花。qRT-PCR显示AtIPK2β会促进FLC的表达。本文进行了染色质免疫共沉淀-qPCR试验,结果表明结合到FLC染色质上。进一步的分析显示AtIPK2β与FLC表观沉默关键基因FVE互作。qRT-PCR,ChIP-qPCR和遗传分析表明AtIPK2β通过抑制FVE在FLC上的积累参与到FVE介导的FLC转录调控。此外,作者发现AtIPK2β还与HDA6相关,HDA6是FVE介导FLC染色质沉默的互作组分,AtIPK2β会减弱HDA6在FLC位点的积累。综上,AtIPK2β通过阻遏FLC的染色质沉默负调控开花时间。




doi: https://doi.org/10.1093/jxb/erx397


Journal: Journal of Experimental Botany
Published data: November 17, 2017.

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