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Renal phosphate transporters.

ABSTRACT: Phosphate homeostasis is tightly controlled by the coordinated activity of bone, kidney, intestine, and parathyroid gland. The renal phosphate transporters have emerged as key regulators of both total body phosphate homeostasis and serum phosphate concentration. This review focuses on the latest updates in phosphate transport and transporters with an emphasis on renal phosphate transporters.Structure function analysis of type II sodium phosphate cotransporters has revealed motifs with significant similarity to those seen in other sodium-coupled solute transporters, identifying key amino acid residues important for solute binding and transport. Previously unidentified regulators of these transporters have been found, although their physiologic significance and interaction with more traditional regulators have not been established. Type II and type III sodium phosphate cotransporters play critical roles in bone, choroid plexus, and vascular physiology and pathophysiology.Increasing knowledge of structure function relationships for sodium phosphate cotransporters, as well as greater appreciation for the complexity of their regulation and role in renal and nonrenal tissue, brings the promise of newer, more specific treatments for disorders of phosphate homeostasis.http://links.lww.com/CONH/A10.

SUBMITTER: Lederer E

PROVIDER: S-EPMC4361807 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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Renal phosphate transporters.

Lederer Eleanor E

Current opinion in nephrology and hypertension 20140901 5

<h4>Purpose of review</h4>Phosphate homeostasis is tightly controlled by the coordinated activity of bone, kidney, intestine, and parathyroid gland. The renal phosphate transporters have emerged as key regulators of both total body phosphate homeostasis and serum phosphate concentration. This review focuses on the latest updates in phosphate transport and transporters with an emphasis on renal phosphate transporters.<h4>Recent findings</h4>Structure function analysis of type II sodium phosphate ...[more]

PMID: 25028980

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Project description:The importance of phosphate (Pi) as an essential component of hydroxyapatite crystals suggests a key role for membrane proteins controlling Pi uptake during mineralization in the tooth. To clarify the involvement of the currently known Pi transporters (Slc17a1, Slc34a1, Slc34a2, Slc34a3, Slc20a1, Slc20a2, and Xpr1) during tooth development and mineralization, we determined their spatiotemporal expression in murine tooth germs from embryonic day 14.5 to postnatal day 15 and in human dental samples from Nolla stages 6 to 9. Using real-time polymerase chain reaction, in situ hybridization, immunohistochemistry, and X-gal staining, we showed that the expression of Slc17a1, Slc34a1, and Slc34a3 in tooth germs from C57BL/6 mice were very low. In contrast, Slc34a2, Slc20a1, Slc20a2, and Xpr1 were highly expressed, mostly during the postnatal stages. The expression of Slc20a2 was 2- to 10-fold higher than the other transporters. Comparable results were obtained in human tooth germs. In mice, Slc34a2 and Slc20a1 were predominantly expressed in ameloblasts but not odontoblasts, while Slc20a2 was detected neither in ameloblasts nor in odontoblasts. Rather, Slc20a2 was highly expressed in the stratum intermedium and the subodontoblastic cell layer. Although Slc20a2 knockout mice did not show enamel defects, mutant mice showed a disrupted dentin mineralization, displaying unmerged calcospherites at the mineralization front. This latter phenotypical finding raises the possibility that Slc20a2 may play an indirect role in regulating the extracellular Pi availability for mineralizing cells rather than a direct role in mediating Pi transport through mineralizing plasma cell membranes. By documenting the spatiotemporal expression of Pi transporters in the tooth, our data support the possibility that the currently known Pi transporters may be dispensable for the initiation of dental mineralization and may rather be involved later during the tooth mineralization scheme.

Project description:Purpose:This study was aimed to profile the transcriptome changes of Toxoplasma after loss of phosphate transporters. For this purpose, phosphate transporter TgPiT and TgPT2 mutants were constructed by using direct knockout or conditional knockdown methods in RH or TATi parasite strain, respectively. The transcriptome changes were captured by RNA-seq analyses. Methods: Transcriptomic profiles of mutants (Δpit and iKD-PT2+ATc, respectively) and controls (RH and iKD-PT2-ATc,respectively) were generated by deep sequencing, in triplicate, using Illumina HiSeq xten. The sequence reads that passed quality filters were analyzed at the transcript level with TopHat (v2.1.1) followed by RSEM (v1.3.3). The differential expression genes were identified by DESeq2 (v1.24.0) analyses (mutant samples versus control samples). Results: Using an optimized data analysis workflow, More than 30 million paired-end reads were generated for each sample and about 90% of the clean reads were mapped to GT1 reference genome. RNA-seq data indicated deletion of TgPiT caused modest transcriptome changes in Toxoplasma. Within the 61 DEGs, several genes are typically increased during transition from tachyzoites to bradyzoites, were upregulated in the Δpit mutant, thus suggest stress response in Toxoplasma due to inactivation of TgPiT. While more than 900 genes (fold change ≥2 and adjusted p value <0.05) were significantly regulated in TgPT2 knockdown mutant. Enrichment of the differentially expressed genes using cluster of orthologous group indicate that these DEGs were enriched in pathways like genetic information processing (such as protein translation, transcription, RNA processing and modification, DNA replication and repair, chromatin structure regulation), nutrient transport and metabolism, signal transduction, intracellular trafficking, protein secretion and vesicular transport etc. 24 of 61 DEGs in Δpit strain were also found in DEGs of TgPT2 deficient parasites. The similar gene expression changes caused by inactivation of TgPiT and TgPT2 suggest that the two proteins have overlapping functions. Conclusions: Our study revealed the transcriptome changes in Toxoplasma due to phosphate transporters deficiency with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here provide the overall transcripts changes in TgPiT and TgPT2 defect strains, respectively. The results showed the unique and overlapping impacts of TgPiT and TgPT2 on Toxoplasma. These widen our understanding of phosphate requirements and potential transport pathway in Toxoplasma.

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Renal phosphate transporters.

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Renal phosphate transporters.

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