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WRKY33 负调控花色素苷生物合成,并与 PHR1 合作介导对磷酸盐饥饿的适应。

WRKY33 negatively regulates anthocyanin biosynthesis and cooperates with PHR1 to mediate acclimation to phosphate starvation.

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 the MOA of China and Zhejiang Province, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China; State Key Laboratory of Subtropical Silviculture, Zhejiang Provincial Key Laboratory of Resources Protection and Innovation of Traditional Chinese Medicine, Zhejiang A&F University, Hangzhou 311300, China.

State Key Laboratory of Subtropical Silviculture, Zhejiang Provincial Key Laboratory of Resources Protection and Innovation of Traditional Chinese Medicine, Zhejiang A&F University, Hangzhou 311300, China.

出版信息

Plant Commun. 2024 May 13;5(5):100821. doi: 10.1016/j.xplc.2024.100821. Epub 2024 Jan 16.

Abstract

Anthocyanin accumulation is acknowledged as a phenotypic indicator of phosphate (Pi) starvation. However, negative regulators of this process and their molecular mechanisms remain largely unexplored. In this study, we demonstrate that WRKY33 acts as a negative regulator of phosphorus-status-dependent anthocyanin biosynthesis. WRKY33 regulates the expression of the gene encoding dihydroflavonol 4-reductase (DFR), a rate-limiting enzyme in anthocyanin production, both directly and indirectly. WRKY33 binds directly to the DFR promoter to repress its expression and also interferes with the MBW complex through interacting with PAP1 to indirectly influence DFR transcriptional activation. Under -Pi conditions, PHR1 interacts with WRKY33, and the protein level of WRKY33 decreases; the repression of DFR expression by WRKY33 is thus attenuated, leading to anthocyanin accumulation in Arabidopsis. Further genetic and biochemical assays suggest that PHR1 is also involved in regulating factors that affect WRKY33 protein turnover. Taken together, our findings reveal that Pi starvation represses WRKY33, a repressor of anthocyanin biosynthesis, to finely tune anthocyanin biosynthesis. This "double-negative logic" regulation of phosphorus-status-dependent anthocyanin biosynthesis is required for the maintenance of plant metabolic homeostasis during acclimation to Pi starvation.

摘要

花色素苷积累被认为是磷(Pi)饥饿的表型指标。然而,该过程的负调控因子及其分子机制在很大程度上仍未被探索。在本研究中,我们证明 WRKY33 作为磷状态依赖性花色素苷生物合成的负调节剂。WRKY33 直接和间接调节花色苷生物合成中限速酶二氢黄酮醇 4-还原酶(DFR)基因的表达。WRKY33 直接结合 DFR 启动子以抑制其表达,并且通过与 PAP1 相互作用干扰 MBW 复合物,从而间接影响 DFR 的转录激活。在低 Pi 条件下,PHR1 与 WRKY33 相互作用,WRKY33 的蛋白水平降低;WRKY33 对 DFR 表达的抑制作用因此减弱,导致拟南芥中花色素苷的积累。进一步的遗传和生化分析表明,PHR1 还参与调节影响 WRKY33 蛋白周转的因素。总之,我们的研究结果表明,Pi 饥饿抑制 WRKY33,即花色苷生物合成的负调控因子,从而精细调节花色苷的生物合成。这种“双负逻辑”调节磷状态依赖性花色素苷生物合成对于植物在适应 Pi 饥饿时维持代谢稳态是必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbe4/11121177/132555ef08fa/gr1.jpg

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