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SPX4与PHR1和PAP1相互作用,以调控磷状态依赖性花青素生物合成中的关键步骤。

SPX4 interacts with both PHR1 and PAP1 to regulate critical steps in phosphorus-status-dependent anthocyanin biosynthesis.

作者信息

He Yuqing, Zhang Xueying, Li Linying, Sun Zongtao, Li Junmin, Chen Xiaoya, Hong Gaojie

机构信息

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Key Laboratory of Biotechnology in Plant Protection of Ministry of Agriculture and Zhejiang Province, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences, 198 Shiqiao Road, Hangzhou, 310021, China.

State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Key Laboratory of Biotechnology in Plant Protection of Ministry of Agriculture and Zhejiang Province, Institute of Plant Virology, Ningbo University, Ningbo, 315211, China.

出版信息

New Phytol. 2021 Apr;230(1):205-217. doi: 10.1111/nph.17139. Epub 2020 Dec 31.

DOI:10.1111/nph.17139
PMID:33617039
Abstract

Phosphate (Pi) is the plant-accessible form of phosphorus, and its insufficiency limits plant growth. The over-accumulation of anthocyanins in plants is often an indication of Pi starvation. However, whether the two pathways are directly linked and which components are involved in this process await identification. Here, we demonstrate that SPX4, a conserved regulator of the Pi response, transduces the Pi starvation signal to anthocyanin biosynthesis in Arabidopsis. When phr1spx4 plants were grown under low Pi conditions, DFR expression and anthocyanin biosynthesis were induced, which distinguished the plant from the behavior reported in the phr1 mutant. We also provide evidence that SPX4 interacts with PAP1, an MYB transcription factor that controls the anthocyanin biosynthetic pathway, in an inositol polyphosphate-dependent manner. Through a physical interaction, SPX4 prevented PAP1 from binding to its target gene promoter; by contrast, during Pi-deficient conditions, in the absence of inositol polyphosphates, PAP1 was released from SPX to activate anthocyanin biosynthesis. Our results reveal a direct link between Pi deficiency and flavonoid metabolism. This new regulatory module, at least partially independent from PHR1, may contribute to developing a strategy for plants to adapt to Pi starvation.

摘要

磷酸盐(Pi)是植物可利用的磷形态,其不足会限制植物生长。植物中花青素的过度积累通常是Pi饥饿的一个指标。然而,这两条途径是否直接相关以及该过程涉及哪些成分尚待确定。在这里,我们证明了SPX4,一种保守的Pi反应调节因子,将Pi饥饿信号传递给拟南芥中的花青素生物合成。当phr1spx4植物在低Pi条件下生长时,DFR表达和花青素生物合成被诱导,这使该植物与phr1突变体中报道的行为有所不同。我们还提供证据表明,SPX4以肌醇多磷酸依赖的方式与PAP1相互作用,PAP1是一种控制花青素生物合成途径的MYB转录因子。通过物理相互作用,SPX4阻止PAP1与其靶基因启动子结合;相反,在Pi缺乏条件下,在没有肌醇多磷酸的情况下,PAP1从SPX中释放出来以激活花青素生物合成。我们的结果揭示了Pi缺乏与类黄酮代谢之间的直接联系。这个新的调节模块至少部分独立于PHR1,可能有助于制定植物适应Pi饥饿的策略。

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