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A family of retroviruses that utilize related phosphate transporters for cell entry.

ABSTRACT: The amphotropic murine retrovirus receptor Ram-1 shows significant sequence similarity to the gibbon ape leukemia virus (GALV) receptor Glvr-1, and both of these cell surface virus receptors normally function as sodium-dependent phosphate symporters. However, Ram-1 from humans or rats does not serve as a receptor for GALV, and Glvr-1 from humans does not serve as a receptor for amphotropic virus. Here we show that the murine retrovirus 10A1 can enter cells by using either Glvr-1 or Ram-1. Furthermore, we have constructed Ram-1/Glvr-1 hybrid receptors that allow entry of both GALV and amphotropic virus. While GALV and amphotropic virus are in separate interference groups when assayed on human cells, they do interfere with each other in cells expressing the hybrid receptor. These results indicate a close functional relationship between retroviruses that utilize members of this newly defined receptor family and provide a molecular explanation for nonreciprocal and cell type-specific interference observed for some retrovirus classes.

SUBMITTER: Miller DG

PROVIDER: S-EPMC237294 | biostudies-other | 1994 Dec

REPOSITORIES: biostudies-other

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A family of retroviruses that utilize related phosphate transporters for cell entry.

Miller D G DG Miller A D AD

Journal of virology 19941201 12

The amphotropic murine retrovirus receptor Ram-1 shows significant sequence similarity to the gibbon ape leukemia virus (GALV) receptor Glvr-1, and both of these cell surface virus receptors normally function as sodium-dependent phosphate symporters. However, Ram-1 from humans or rats does not serve as a receptor for GALV, and Glvr-1 from humans does not serve as a receptor for amphotropic virus. Here we show that the murine retrovirus 10A1 can enter cells by using either Glvr-1 or Ram-1. Furthe ...[more]

PMID: 7966619

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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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A family of retroviruses that utilize related phosphate transporters for cell entry.

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A family of retroviruses that utilize related phosphate transporters for cell entry.

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