| Summary: | 博士 === 國立中興大學 === 生物科技學研究所 === 102 === Members of the Arabidopsis PHOSPHATE TRANSPORTER 1 (PHT1) family are key players in acquisition of phosphate (Pi) from the rhizosphere, and their regulation is indispensable for the maintenance of cellular Pi homeostasis. In this study, we revealed regulation of Pi transport, through post-translational modulation and degradation of PHT1 proteins by the RING-type ubiquitin E3 ligase, NITROGEN LIMITATION ADAPTATION (NLA). Loss-of-function of NLA caused high Pi accumulation resulting from increases in the levels of several PHT1s at the protein rather than the transcript level. Evidence of decreased endocytosis and ubiquitination of PHT1s in nla mutants and interaction between NLA and PHT1s in the plasma membranes suggests that NLA directs the ubiquitination of plasma membrane-localized PHT1s which triggers clathrin-dependent endocytosis followed by endosomal sorting to vacuoles. Further, different subcellular localization of NLA and PHO2 and synergistic effect of the accumulation of PHT1s and Pi in nla pho2 mutants suggest that they function independently but cooperatively to control PHT1 protein amounts. Intriguingly, NLA and PHO2 are the targets of two Pi starvation-induced microRNAs, miR827 and miR399, respectively. Our findings, therefore, uncover modulation of Pi transport activity in response to Pi availability through the integration of miRNA-mediated post-transcriptional and ubiquitin-mediated post-translational regulation.
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