Li Huiqiong, He Kunrong, Zhang ZhiQiang, Hu Yanru
CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China; Yunnan Key Laboratory of Plant Reproductive Adaptation and Evolutionary Ecology, Institute of Biodiversity, School of Ecology and Environmental Science, Yunnan University, Kunming, 650504, Yunnan, China.
CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China; Center of Economic Botany, Core Botanical Gardens, Chinese Academy of Sciences, Kunming, Yunnan, 650223, China; University of Chinese Academy of Sciences, Beijing, 100049, China.
Plant Physiol Biochem. 2023 Mar;196:121-129. doi: 10.1016/j.plaphy.2023.01.029. Epub 2023 Jan 16.
Anthocyanins, flavonoid compounds derived from secondary metabolic pathways, play important roles in various biological processes. Phosphorus (P) is an essential macroelement for plant growth and development, and P-starvation usually results in anthocyanin accumulation. However, the molecular mechanism of P deficiency promotes anthocyanin biosynthesis has not been well characterized. Here, we provided evidence that the P signaling core protein PHOSPHATE STARVATION RESPONSE1 (PHR1) is physically associate with transcription factors (TFs) involved in anthocyanidin biosynthesis, including PRODUCTION OF ANTHOCYANIN PIGMENTS1 (PAP1/MYB75), MYB DOMAIN PROTEIN 113 (MYB113) and TRANSPARENT TESTA 8 (TT8). PHR1 and its homologies positively regulated anthocyanin accumulation in Arabidopsis seedlings under P-deficient conditions. Disruption of PHR1 simultaneously rendered seedlings hyposensitive to limiting P, whereas the overexpression of PHR1 enhanced P- deficiency-induced anthocyanin accumulation. Genetic analysis demonstrated that 35S:PHR1-2HA-5 seedlings partially recovers the P deficiency insensitive phenotype of myb-RNAi and tt8 mutants. In summary, our study indicated that protein complexes formed by PHR1 and MBW complex directly mediate the process of P-deficiency-induced anthocyanin accumulation, providing a new mechanistic understanding of how P-deficient signaling depends on the endogenous anthocyanin synthesis pathway to promote anthocyanin accumulation in Arabidopsis.
花青素是次生代谢途径衍生的类黄酮化合物，在各种生物过程中发挥重要作用。磷（P）是植物生长发育必需的大量元素，缺磷通常会导致花青素积累。然而，磷缺乏促进花青素生物合成的分子机制尚未得到充分表征。在这里，我们提供了证据表明磷信号核心蛋白磷饥饿反应1（PHR1）与参与花青素生物合成的转录因子（TFs）存在物理关联，包括花青素色素产生1（PAP1/MYB75）、MYB结构域蛋白113（MYB113）和透明种皮8（TT8）。在缺磷条件下，PHR1及其同源物正向调节拟南芥幼苗中的花青素积累。PHR1的破坏同时使幼苗对低磷不敏感，而PHR1的过表达增强了缺磷诱导的花青素积累。遗传分析表明，35S:PHR1-2HA-5幼苗部分恢复了myb-RNAi和tt8突变体的缺磷不敏感表型。总之，我们的研究表明，由PHR1和MBW复合物形成的蛋白质复合物直接介导了缺磷诱导的花青素积累过程，为缺磷信号如何依赖内源性花青素合成途径促进拟南芥中花青素积累提供了新的机制理解。
