高亲和力磷酸盐(Pi)转运蛋白(PHTs)PHT1;1和PHT1;4是植物根Pi吸收所必需的,尤其是在Pi缺乏的条件下,但是如何调节它们的蛋白质稳定性仍然难以捉摸。这里,我们鉴定了一个TtransferDNA插入突变体SortingNexin1(SNX1),在缺乏Pi的情况下,比野生型具有更多的Pi含量和更少的花青素积累。相比之下,snx1-2突变体在种子萌发和根伸长方面对外源砷酸盐表现出更高的敏感性,揭示较高的Pi摄取率。进一步的研究表明,SNX1可以与PHT1共定位并相互作用。1和PHT1;4在囊泡和质膜上。遗传分析表明,在低Pi条件下,snx1-2突变体中Pi含量的增加可能会通过突变PHT1而受到广泛损害;双突变体snx1-2pht1中的1;1,表明SNX1对PHT1具有上位性;1。此外,SNX1负控制PHT1;1蛋白质稳定性;因此,在足够或缺乏Pi的情况下,snx1-2突变体与野生型相比,质膜中的PHT1;1蛋白丰度增加。一起,我们的研究(i)确定SNX1是植物对低Pi反应的关键调节剂,(ii)揭示其在PHT1调节中的作用;1蛋白质稳定性,PHT1;1在质膜上积累,和根Pi吸收。
High-affinity phosphate (Pi) transporters (PHTs) PHT1;1 and PHT1;4 are necessary for plant root Pi uptake especially under Pi-deficient conditions, but how their protein stability is modulated remains elusive. Here, we identified a Ttransfer DNA insertion mutant of Sorting Nexin1 (
SNX1), which had more Pi content and less anthocyanin accumulation than the wild type under deficient Pi. By contrast, the snx1-2 mutant displayed higher sensitivity to exogenous arsenate in terms of seed germination and root elongation, revealing higher Pi uptake rates. Further study showed that
SNX1 could co-localize and interact with PHT1;1 and PHT1;4 in vesicles and at the plasma membrane. Genetic analysis showed that increased Pi content in the
snx1-2 mutant under low Pi conditions could be extensively compromised by mutating PHT1;1 in the double mutant
snx1-2 pht1;1, revealing that
SNX1 is epistatic to PHT1;1. In addition,
SNX1 negatively controls PHT1;1 protein stability; therefore, PHT1;1 protein abundance in the plasma membrane was increased in the snx1-2 mutant compared with the wild type under either sufficient or deficient Pi. Together, our study (i) identifies SNX1 as a key modulator of the plant response to low Pi and (ii) unravels its role in the modulation of PHT1;1 protein stability, PHT1;1 accumulation at the plasma membrane, and root Pi uptake.