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磷酸盐 1 介导的从根部到地上部的磷酸盐转运调节植物的花发育转变。

PHOSPHATE1-mediated phosphate translocation from roots to shoots regulates floral transition in plants.

机构信息

College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou 311121, China.

Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai, China.

出版信息

J Exp Bot. 2024 Aug 28;75(16):5054-5075. doi: 10.1093/jxb/erae222.

Abstract

Phosphorus nutrition has been known for a long time to influence floral transition in plants, but the underlying mechanism is unclear. Arabidopsis phosphate transporter PHOSPHATE1 (PHO1) plays a critical role in phosphate translocation from roots to shoots, but whether and how it regulates floral transition is unknown. Here, we show that knockout mutation of PHO1 delays flowering under both long- and short-day conditions. The late flowering of pho1 mutants can be partially rescued by Pi supplementation in rosettes or shoot apices. Grafting assay indicates that the late flowering of pho1 mutants is a result of impaired phosphate translocation from roots to shoots. Knockout mutation of SPX1 and SPX2, two negative regulators of the phosphate starvation response, partially rescues the late flowering of pho1 mutants. PHO1 is epistatic to PHO2, a negative regulator of PHO1, in flowering time regulation. Loss of PHO1 represses the expression of some floral activators, including FT encoding florigen, and induces the expression of some floral repressors in shoots. Genetic analyses indicate that at least jasmonic acid signaling is partially responsible for the late flowering of pho1 mutants. In addition, we find that rice PHO1;2, the homolog of PHO1, plays a similar role in floral transition. These results suggest that PHO1 integrates phosphorus nutrition and flowering time, and could be used as a potential target in modulating phosphorus nutrition-mediated flowering time in plants.

摘要

磷营养长期以来被认为会影响植物的花发育转变,但潜在的机制尚不清楚。拟南芥磷酸盐转运蛋白 PHOSPHATE1(PHO1)在磷酸盐从根部向地上部的转运中起着关键作用,但它是否以及如何调节花发育转变尚不清楚。在这里,我们表明 PHO1 的敲除突变会延迟长日和短日条件下的开花。在莲座叶或茎尖中补充 Pi 可部分挽救 pho1 突变体的晚花表型。嫁接实验表明, pho1 突变体的晚花表型是由于根部向地上部的磷酸盐转运受损所致。磷酸盐饥饿反应的两个负调控因子 SPX1 和 SPX2 的敲除突变体部分挽救了 pho1 突变体的晚花表型。在开花时间调控中,PHO1 对 PHO2(PHO1 的负调控因子)具有上位性。PHO1 的缺失抑制了一些花激活因子的表达,包括作为成花素的 FT 编码基因,并诱导地上部一些花抑制因子的表达。遗传分析表明,至少茉莉酸信号通路部分负责 pho1 突变体的晚花表型。此外,我们发现水稻 PHO1;2,PHO1 的同源物,在花发育转变中也起着类似的作用。这些结果表明 PHO1 整合了磷营养和开花时间,并且可以作为调节植物中磷营养介导的开花时间的潜在靶标。

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