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Gene Review

Slc13a1  -  solute carrier family 13 (sodium/sulfate...

Mus musculus

Synonyms: AI314066, AI987826, Na(+)/sulfate cotransporter, NaSi-1, Nas1, ...
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Disease relevance of Slc13a1

  • Spontaneous clonic seizures were observed in Nas1-/- mice from 8 months of age [1].
  • Nas1-/- mouse body weight was reduced by >20% when compared with Nas1+/+ and Nas1+/- littermates at 2 weeks of age and remained so throughout adulthood [1].
  • We previously generated a NaS1 knockout (Nas1-/-) mouse, an animal model for hyposulfatemia, that exhibits reduced growth and liver abnormalities including hepatomegaly [2].

Psychiatry related information on Slc13a1

  • There were no significant differences between Nas1-/- and Nas1+/+ mice in the cookie test after moderate food deprivation [3].
  • The Nas1-/- mice displayed significantly (P<0.05) increased latencies to find an escape platform in the reversal learning trials at 2 days but not 1 day after the last acquisition trial in a Morris water maze test, suggesting that Nas1-/- mice may have proactive memory interference [3].
  • The Nas1-/- mice also displayed decreased locomotor activity by moving less distance (1.53 +/- 0.27 m, P < 0.05) in an open-field test when compared to Nas1+/+ (2.31 +/- 0.24 m) and Nas1+/- (2.15 +/- 0.19 m) mice [4].
  • In addition, both Nas1-/- and Nas1+/+ mice displayed similar escape latencies in the acquisition phase of the Morris water maze test, suggesting that learning, motivation, vision and motor skills required for the task may not be affected in Nas1-/- mice [3].

High impact information on Slc13a1

  • Nas1-/- mice exhibit increased urinary sulfate excretion, reduced renal and intestinal Na+-SO42- cotransport, and a general growth retardation [1].
  • These data demonstrate NaSi-1 is essential for maintaining sulfate homeostasis, and its expression is necessary for a wide range of physiological functions [1].
  • Nas1-/- females had a lowered fertility, with a 60% reduction in litter size [1].
  • In the present study, we identified two loss-of-function polymorphisms in the human NaS1 gene and showed the Nas1-null mouse to be hypersensitive to APAP hepatotoxicity [5].
  • APAP treatment led to increased liver damage and decreased hepatic glutathione levels in the hyposulfatemic Nas1-null mice compared with that in normosulfatemic wild-type mice [5].

Biological context of Slc13a1

  • The mouse Na(+)-sulfate cotransporter gene Nas1. Cloning, tissue distribution, gene structure, chromosomal assignment, and transcriptional regulation by vitamin D [6].
  • The Nas1 gene is a single copy gene comprising 15 exons spread over 75 kilobase pairs that maps to mouse chromosome 6 [6].
  • To understand the molecular mechanisms that mediate the regulation of NaSi-1, we have isolated and characterized the mouse NaSi-1 cDNA (mNaSi-1), gene (Nas1), and promoter region and determined Nas1 chromosomal localization [6].
  • The three genotypes displayed similar spatiotemporal and ethological behaviours in the elevated-plus maze and open-field test, with the exception of a decreased defecation frequency by the Nas1-/- mice (40% reduction, P < 0.01) [4].
  • Mutational analysis of the Nas1 promoter resulted in identification of a direct repeat 6-type vitamin-D-responsive element (DR6 VDRE) at -525 to -508 and an imperfect inverted repeat 0-type T(3)-responsive element (IR0 T(3)RE) at -436 to -425 which conferred 1,25-(OH)(2)D(3) and T(3) responsiveness, respectively [7].

Anatomical context of Slc13a1

  • The concentration of NaSi-1 transporter protein in crude membrane isolated from rat kidney cortex was 0.094+/-0.014 fmol/ microg protein (mean+/-SD of three preparations) [8].

Associations of Slc13a1 with chemical compounds

  • Regulation of the mouse Nas1 promoter by vitamin D and thyroid hormone [7].
  • Vitamin D (1,25-(OH)2D3) and thyroid hormone (T3) led to an increase in Nas1 promoter activity in OK cells [9].
  • Analysis of urinary APAP metabolites revealed a significantly lower ratio of APAP-sulfate to APAP-glucuronide in the Nas1-null mice [5].
  • In addition, Nas1-/- mice exhibited increased levels of hepatic lipid (approximately 16% increase), serum cholesterol (approximately 20% increase), and low-density lipoprotein (approximately 100% increase) and reduced hepatic glycogen (approximately 50% decrease) levels [2].

Other interactions of Slc13a1

  • Impaired memory and olfactory performance in NaSi-1 sulphate transporter deficient mice [3].
  • Similar results were observed in VDR knockout mice after their blood ionized calcium levels and rachitic bone phenotype were normalized by dietary means, indicating that vitamin D regulation of NaSi-1 expression and sulfate metabolism is independent of its role in calcium metabolism [10].

Analytical, diagnostic and therapeutic context of Slc13a1

  • In the present study, NaSi-1 sulphate transporter knock-out (Nas1-/-) mice, an animal model of hyposulphataemia, were examined for spatial memory and learning in a Morris water maze, and for olfactory function in a cookie test [3].
  • There were no significant differences between Nas1-/- and Nas1+/+ mice in a rotarod performance test of motor coordination and in the forced swim test assessing (anti-)depressant-like behaviours [4].
  • Using the purified monoclonal antibody as the capture antibody and the polyclonal antibody as the detecting antibody, a simple and sensitive sandwich-type enzyme-linked immunosorbent assay was developed to quantitate NaSi-1 transporter protein levels in tissue [8].
  • In this study, we investigated the hepatic gene expression profile of Nas1-/- mice using oligonucleotide microarrays [2].


  1. Hyposulfatemia, growth retardation, reduced fertility, and seizures in mice lacking a functional NaSi-1 gene. Dawson, P.A., Beck, L., Markovich, D. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  2. Transcriptional profile reveals altered hepatic lipid and cholesterol metabolism in hyposulfatemic NaS1 null mice. Dawson, P.A., Gardiner, B., Grimmond, S., Markovich, D. Physiol. Genomics (2006) [Pubmed]
  3. Impaired memory and olfactory performance in NaSi-1 sulphate transporter deficient mice. Dawson, P.A., Steane, S.E., Markovich, D. Behav. Brain Res. (2005) [Pubmed]
  4. Behavioural abnormalities of the hyposulphataemic Nas1 knock-out mouse. Dawson, P.A., Steane, S.E., Markovich, D. Behav. Brain Res. (2004) [Pubmed]
  5. Disruption of NaS1 sulfate transport function in mice leads to enhanced acetaminophen-induced hepatotoxicity. Lee, S., Dawson, P.A., Hewavitharana, A.K., Shaw, P.N., Markovich, D. Hepatology (2006) [Pubmed]
  6. The mouse Na(+)-sulfate cotransporter gene Nas1. Cloning, tissue distribution, gene structure, chromosomal assignment, and transcriptional regulation by vitamin D. Beck, L., Markovich, D. J. Biol. Chem. (2000) [Pubmed]
  7. Regulation of the mouse Nas1 promoter by vitamin D and thyroid hormone. Dawson, P.A., Markovich, D. Pflugers Arch. (2002) [Pubmed]
  8. Detection and quantitation of a sodium-dependent sulfate cotransporter (NaSi-1) by sandwich-type enzyme-linked immunosorbent assay. Sagawa, K., DuBois, D.C., Han, B., Almon, R.R., Biber, J., Murer, H., Morris, M.E. Pflugers Arch. (1998) [Pubmed]
  9. Transcriptional regulation of the sodium-sulfate cotransporter NaS(i)-1 gene. Dawson, P.A., Markovich, D. Cell Biochem. Biophys. (2002) [Pubmed]
  10. Critical role of vitamin D in sulfate homeostasis: regulation of the sodium-sulfate cotransporter by 1,25-dihydroxyvitamin D3. Bolt, M.J., Liu, W., Qiao, G., Kong, J., Zheng, W., Krausz, T., Cs-Szabo, G., Sitrin, M.D., Li, Y.C. Am. J. Physiol. Endocrinol. Metab. (2004) [Pubmed]
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