磷是植物生长发育的所必需的大量元素之一。植物在低磷条件下生长时，根构型会发生重塑， 以有利于更好地吸收土壤养分。这一重塑过程包括主根的生长受到抑制，并形成大量的侧根。但目前关于低磷信号是如何调控根构型重塑的分子机制并不清楚。在前期的工作中， 我们获得了一个对低磷胁迫诱导的根构型重塑超敏的拟南芥突变体hps10。分子遗传学分析表明，HPS10和另一个蛋白AtSTAR1共同组成一个位于液泡膜上的ABC转运复合体(ATP-binding cassette transport complex)。 本项目将通过深入分析这一转运复合体的生化功能和转运调控机制，克隆其遗传抑制子基因，鉴定其互作蛋白等，来全面探究低磷胁迫诱导根构型重塑的分子机制。此外，我们还获得了一批新的影响低磷诱导根构型重塑的突变体。对这些突变基因的克隆鉴定也将为阐明低磷胁迫诱导根构型重塑的分子机制提供新的线索。

Phosphorus is an essential macronutrient for plant growth and development. When grown under phosphate (Pi) starvation, plants exhibits a remodelling of root architecture to increase Pi uptake. This remodelling process includes the inhibition of primary root growth and the enhancement of lateral root growth. The molecular mechanism underlying this change, however, is not understood. Previously, we identified an Arabidopsis mutant, hps10, which is hypersensitive to Pi starvation-induced remodelling of root architecture. Molecular and genetic analyses show that HPS10 and its associated protein AtSTAR1 form an ABC (ATP-binding cassette) transport complex which is localized in tonoplasts. The aim of this research is to understand the molecular mechanism of how Pi starvation induces the remodelling of root architecture by characterizing the biochemical and physiological functions of the HPS10/AtSTAR1 transport complex, identifying its genetic suppressor genes and other interacting proteins, etc. Besides, we have obtained several new Arabidopsis mutants defective in Pi starvation-induced remodelling of root architecture. The cloning of the genes responsible for these mutants will also provide new clues for the molecular mechanism for Pi starvation-induced remodelling of root architecture.