GO:0015709 thiosulfate transport: Mechanism, Genes, Functions and Research Methods

Research-grade guide for scientists and biopharma professionals

Key Takeaways

GO:0015709 thiosulfate transport describes the directed movement of thiosulfate into, out of, or within a cell, or between cells, by means of a transporter or pore.
Thiosulfate transport is best characterized in bacteria, where it fuels electron transport and energy conservation during mixotrophic and chemolithotrophic growth.
In mammals, thiosulfate transport occurs in the kidney proximal tubule and competes with sulfate and oxalate handling, linking it to nephrolithiasis biology.
The process is relevant to host-microbe interactions, including gut inflammation where thiosulfate respiration supports Salmonella expansion.
Key proteins include bacterial thiosulfate-oxidizing systems and mammalian sulfate/anion transporters such as SLC13A1 and SLC26A6.
CRISPR knockout, point-mutation, knock-in, and overexpression models enable causal testing of thiosulfate transport genes in microbial and mammalian systems.

Description

Thiosulfate transport (GO:0015709) is the directed movement of thiosulfate into, out of, or within a cell, or between cells, by means of some agent such as a transporter or pore. Thiosulfate is a sulfur oxyanion that serves as an electron donor for chemolithotrophic and mixotrophic bacteria, and as a sulfur source or competing anion in mammalian epithelia. Because thiosulfate participates in both energy metabolism and sulfur trafficking, its transport is a focal point for understanding microbial bioenergetics and host anion homeostasis. In bacteria such as Thiomonas bhubaneswarensis and Thiobacillus novellus, thiosulfate oxidation is coupled to electron transport chains that conserve energy. In mammals, bidirectional active transport of thiosulfate has been demonstrated in the proximal convolution of the rat kidney, where it interacts with sulfate and oxalate transport pathways. These findings place thiosulfate transport at the intersection of microbial physiology and renal solute handling. For researchers, GO:0015709 provides a precise annotation target for genes encoding transporters, pores, and accessory proteins that mediate thiosulfate flux. Understanding this process supports studies of sulfur metabolism, host-microbe competition, and kidney stone disease mechanisms.

thiosulfate transport At A Glance

GO ID GO:0015709
GO term thiosulfate transport
Ontology biological_process
Synonym thiosulphate transport
Definition The directed movement of thiosulfate into, out of or within a cell, or between cells, by means of some agent such as a transporter or pore.
Major function Mediates thiosulfate flux across membranes for energy metabolism, sulfur acquisition, and anion homeostasis.
Taxonomic scope Documented in bacteria and mammals, including Thiomonas, Thiobacillus, Salmonella, rat kidney, and insect models.
Related anions Sulfate and oxalate transport pathways intersect with thiosulfate handling in renal and epithelial systems.

What Is GO:0015709?

GO:0015709 thiosulfate transport is defined as the directed movement of thiosulfate into, out of, or within a cell, or between cells, by means of some agent such as a transporter or pore. The synonym thiosulphate transport reflects the alternative spelling of the substrate. This biological process encompasses both influx and efflux across membranes and can be mediated by dedicated transporters or anion exchange systems.

Why Is thiosulfate transport Important in Cell Biology?

Thiosulfate transport is important because it connects sulfur oxyanion availability to energy conservation in bacteria and to anion homeostasis in mammals. In microbial systems, thiosulfate oxidation and electron transport support growth and can influence host-microbe interactions during inflammation. In mammals, thiosulfate transport in the kidney proximal tubule competes with sulfate and oxalate, making it relevant to nephrolithiasis and renal solute handling. Thus, GO:0015709 is a key annotation for studies spanning bioenergetics, infectious disease, and kidney physiology.
Supports bacterial energy conservation through thiosulfate oxidation and electron transport.
Enables sulfur acquisition and cysteine biosynthesis in some bacterial species.
Contributes to host-microbe competition during gut inflammation, where thiosulfate respiration supports Salmonella.
Mediates bidirectional active transport in the kidney proximal tubule.
Intersects with sulfate transport via SLC13A1 and related anion transporters.
Modulates oxalate transport through SLC26A6-dependent mechanisms in insect models of calcium oxalate nephrolithiasis.
Provides a target for CRISPR-based functional studies of transporter genes.
Links microbial sulfur metabolism to human disease-relevant anion handling.

What Happens During thiosulfate transport?

Substrate recognition and binding
In simple terms: The transporter first recognizes thiosulfate and binds it specifically.
Thiosulfate transport begins with substrate recognition by a membrane protein or pore complex. In bacteria, thiosulfate oxidation systems couple substrate handling to electron transport, indicating that thiosulfate is recognized and processed at the membrane interface. In mammalian epithelia, thiosulfate transport is saturable and can be bidirectional, implying specific binding sites that distinguish thiosulfate from related anions such as sulfate and oxalate.
Membrane translocation
In simple terms: The bound thiosulfate is moved across the membrane.
After binding, thiosulfate is translocated across the lipid bilayer by a transporter or pore. In the rat kidney proximal convolution, thiosulfate undergoes bidirectional active transport, demonstrating that translocation is carrier-mediated and energy-dependent. In bacteria, thiosulfate movement is linked to electron transport chains that generate a proton motive force or reduce terminal acceptors.
Coupling to electron transport and energy conservation
In simple terms: In bacteria, moving thiosulfate helps the cell make energy.
In obligately mixotrophic and chemolithotrophic bacteria, thiosulfate oxidation is coupled to electron transport, allowing energy conservation. Thiomonas bhubaneswarensis strain S10 oxidizes thiosulfate via a mechanism that feeds electrons into respiratory chains. Thiobacillus novellus similarly couples thiosulfate oxidation to electron transport. This coupling makes thiosulfate transport a bioenergetic process, not merely a nutrient uptake step.
Anion exchange and competition in mammalian epithelia
In simple terms: In the kidney, thiosulfate competes with other anions like sulfate and oxalate.
In mammalian systems, thiosulfate transport intersects with sulfate and oxalate handling. The Na+-sulfate cotransporter SLC13A1 mediates sulfate transport, and thiosulfate can interact with sulfate transport pathways. In an insect model of calcium oxalate nephrolithiasis, sulfate and thiosulfate inhibit oxalate transport via a dPrestin (Slc26a6)-dependent mechanism, showing that thiosulfate competes with oxalate for a shared anion exchange route. These interactions define thiosulfate transport as part of a broader anion homeostasis network.
Physiological consequences of thiosulfate flux
In simple terms: Moving thiosulfate changes what the cell or organism can do.
Thiosulfate flux supports bacterial growth and sulfur metabolism, contributes to cysteine biosynthesis in Neisseria species, and can provide a respiratory electron acceptor for Salmonella during gut inflammation. In mammals, thiosulfate transport in the proximal tubule influences renal anion handling and stone-forming potential. Thus, the physiological output of GO:0015709 depends on the organism and tissue context.

Key Genes Involved in GO:0015709 thiosulfate transport

The following genes and proteins have been experimentally linked to thiosulfate transport or its physiological consequences.
GeneMajor RoleResearch Relevance
Thiomonas bhubaneswarensis S10 thiosulfate oxidation systemOxidizes thiosulfate and feeds electrons into respiratory chainsModel for mixotrophic thiosulfate bioenergetics
Thiobacillus novellus thiosulfate oxidase systemCouples thiosulfate oxidation to electron transportClassic chemolithotrophic model
SLC13A1Na+-sulfate cotransporter; sulfate transport intersects with thiosulfate handlingMammalian anion transport studies
SLC26A6 (dPrestin)Anion exchanger mediating oxalate transport inhibited by sulfate and thiosulfateNephrolithiasis and anion competition models
Salmonella thiosulfate respiration genesUse thiosulfate as a respiratory electron acceptor during gut inflammationHost-microbe interaction and infection models
Neisseria cysteine biosynthesis genesSupport cysteine biosynthesis from sulfur sourcesBacterial sulfur metabolism studies
Molybdate transport genesRelated oxyanion transport system providing comparative contextComparative transporter research
Rat kidney proximal tubule thiosulfate transporterMediates bidirectional active thiosulfate transportRenal physiology and transport kinetics
Sulfate transporter family membersTransport sulfate and related oxyanionsAnion transport specificity studies
Oxalate transporter (Slc26a6)Transports oxalate; inhibited by thiosulfateKidney stone disease models
Bacterial electron transport chain componentsAccept electrons from thiosulfate oxidationBioenergetics and respiration research
Thiosulfate-oxidizing enzyme complexesCatalyze thiosulfate oxidation at the membraneEnzyme mechanism studies
Host inflammatory response genesCreate conditions favoring thiosulfate respiration in SalmonellaInfection and inflammation research
Cysteine biosynthesis pathway genesUtilize sulfur from thiosulfate for cysteine productionMetabolic pathway engineering
Anion exchange proteinsMediate competition between thiosulfate, sulfate, and oxalateTransport competition assays
Renal proximal tubule transport proteinsCarry out active thiosulfate reabsorption or secretionKidney function studies

How Is thiosulfate transport Regulated?

Thiosulfate transport is regulated by substrate availability, competing anions, and the metabolic state of the cell. In bacteria, expression of thiosulfate oxidation and electron transport components is linked to respiratory conditions and growth mode. In Salmonella, gut inflammation provides a respiratory electron acceptor environment that favors thiosulfate respiration. In mammalian epithelia, thiosulfate transport is influenced by sulfate and oxalate concentrations, as shown by competition experiments in kidney and insect models. SLC13A1-mediated sulfate transport provides a related regulatory context for anion handling.

thiosulfate transport and Human Disease

GeneDisease / BiologyPotential Experimental Model
SLC26A6 (dPrestin)Calcium oxalate nephrolithiasis; oxalate transport inhibited by thiosulfateInsect nephrolithiasis model; CRISPR knockout of Slc26a6
SLC13A1Sulfate transport and anion homeostasisMammalian cell lines with SLC13A1 knockout or overexpression
Salmonella thiosulfate respiration genesGut inflammation and infectionMouse infection models with bacterial gene knockouts
Neisseria cysteine biosynthesis genesBacterial sulfur metabolism and survivalNeisseria knockout strains for cysteine biosynthesis
Thiomonas thiosulfate oxidation systemMixotrophic bioenergeticsBacterial knockout and complementation studies
Kidney stone disease and anion transport competition
Thiosulfate transport intersects with oxalate handling in the kidney. In an insect model of calcium oxalate nephrolithiasis, sulfate and thiosulfate inhibit oxalate transport via a dPrestin (Slc26a6)-dependent mechanism. This suggests that thiosulfate availability could modulate stone-forming risk through competition at shared anion exchange routes. The Na+-sulfate cotransporter SLC13A1 further links sulfate and thiosulfate handling in renal epithelia.
Infectious disease and gut inflammation
Gut inflammation provides a respiratory electron acceptor for Salmonella, and thiosulfate respiration supports its expansion. This connects thiosulfate transport and metabolism to host-microbe competition during infection. Understanding how Salmonella accesses and utilizes thiosulfate may inform strategies to limit pathogen growth in inflamed gut environments.
Bacterial sulfur metabolism and cysteine biosynthesis
In Neisseria species, cysteine biosynthesis depends on sulfur acquisition pathways that can involve thiosulfate. Disruption of these pathways affects bacterial survival and may represent a target for antimicrobial development. Thiosulfate oxidation in Thiomonas and Thiobacillus further illustrates the importance of sulfur oxyanion handling for bacterial energy metabolism.

From thiosulfate transport-Related Genes to Experimental Models

Research QuestionSuitable Model
Does a candidate transporter mediate thiosulfate uptake?CRISPR knockout in bacterial or mammalian cells followed by transport assays
Does a point mutation alter substrate specificity?CRISPR point-mutation knock-in of transporter active-site residues
Can a tagged transporter be localized in live cells?Knock-in of fluorescent or epitope tags at the endogenous locus
Does overexpression increase thiosulfate flux?CRISPR activation or cDNA overexpression in cell lines
Does thiosulfate transport affect host-microbe competition?Bacterial knockout in infection models with inflammatory challenge
Does thiosulfate compete with oxalate in vivo?Animal or insect models with transporter knockouts

How to Study the thiosulfate transport Process

MethodWhat It MeasuresTypical Application
Radiolabeled thiosulfate flux assayDirectional transport ratesKidney proximal tubule transport studies
Anion competition assaySpecificity and inhibition by sulfate or oxalateNephrolithiasis and anion exchange research
Bacterial gene knockout and complementationRequirement of genes for thiosulfate oxidationBioenergetics and sulfur metabolism
Infection model with bacterial mutantsContribution of thiosulfate respiration to colonizationSalmonella gut inflammation studies
RNA-seqExpression of transport and metabolic genesHost-microbe interaction transcriptomics
ProteomicsProtein abundance of transporter complexesBacterial electron transport chain analysis
Fluorescence imagingSubcellular localization of tagged transportersMammalian epithelial transport studies
CRISPR knockout screeningCausal role of candidate transport genesFunctional genomics of anion transport
Transport assays with radiolabeled or fluorescent thiosulfate
Direct measurement of thiosulfate flux can be performed using radiolabeled or fluorescent analogs in cell and membrane vesicle systems. Bidirectional active transport of thiosulfate was demonstrated in the rat kidney proximal convolution using such approaches. These assays distinguish influx from efflux and can test competition with sulfate and oxalate.
Genetic knockout and complementation in bacteria
Bacterial genetics allows deletion of candidate thiosulfate oxidation or transport genes followed by complementation. Studies in Thiomonas bhubaneswarensis and Thiobacillus novellus used such approaches to link thiosulfate oxidation to electron transport. Similar strategies can test Salmonella thiosulfate respiration genes during infection.
Anion competition and inhibitor studies
Because thiosulfate competes with sulfate and oxalate, competition assays are valuable for defining transporter specificity. In an insect nephrolithiasis model, sulfate and thiosulfate inhibited oxalate transport via a dPrestin (Slc26a6)-dependent mechanism. SLC13A1 studies provide a framework for analyzing Na+-dependent sulfate transport and its interaction with thiosulfate.
Expression and localization analysis
RNA-seq, proteomics, and imaging can reveal where and when thiosulfate transport components are expressed. In Salmonella, inflammatory conditions induce a respiratory program that includes thiosulfate utilization. In mammalian kidney, proximal tubule localization of thiosulfate transport activity has been established by functional studies.

How CRISPR Can Be Used to Study GO:0015709 thiosulfate transport

Knockout

CRISPR knockout of candidate thiosulfate transport genes can test whether they are required for thiosulfate flux or downstream phenotypes. In bacteria, deletion of thiosulfate oxidation genes followed by complementation has been used to link thiosulfate metabolism to electron transport. In mammalian cells, knockout of SLC26A6 or SLC13A1 can reveal their contributions to anion competition and oxalate handling.

Point Mutation

Point mutations in transporter active sites can define residues required for thiosulfate recognition and translocation. CRISPR point-mutation knock-in allows testing of specific amino acid changes without altering gene expression. Such experiments are valuable for distinguishing thiosulfate from sulfate and oxalate transport.

Knock-in

Knock-in of epitope or fluorescent tags at endogenous loci enables real-time localization and interaction studies of thiosulfate transporters. Tagged knock-in models can be used to track transporter trafficking in kidney epithelial cells or bacteria. This approach preserves native regulatory context.

Overexpression

Overexpression of candidate transporters can increase thiosulfate flux and amplify phenotypes for biochemical assays. CRISPR activation or cDNA overexpression has been used to study anion transport proteins such as SLC13A1. In bacteria, overexpression of thiosulfate oxidation components can enhance electron transport activity.

How EDITGENE Supports thiosulfate transport Research

Researchers studying thiosulfate transport-related genes often need to determine whether a candidate gene is causally involved in thiosulfate flux, anion competition, or host-microbe interactions. EDITGENE provides CRISPR-based cell models and screening services to test these hypotheses with publication-grade rigor.
Contact EDITGENE today to design your custom CRISPR model for thiosulfate transport research.

Frequently Asked Questions About thiosulfate transport

GO:0015709 thiosulfate transport is the directed movement of thiosulfate into, out of, or within a cell, or between cells, by means of a transporter or pore.
Genes include bacterial thiosulfate oxidation systems in Thiomonas and Thiobacillus, Salmonella thiosulfate respiration genes, and mammalian anion transporters such as SLC13A1 and SLC26A6.
In the rat kidney proximal tubule, thiosulfate transport is bidirectional and active, indicating carrier-mediated and energy-dependent movement.
Sulfate and thiosulfate inhibit oxalate transport via a dPrestin (Slc26a6)-dependent mechanism, linking thiosulfate handling to calcium oxalate nephrolithiasis.
Yes, thiosulfate oxidation and transport are coupled to electron transport in bacteria such as Thiomonas bhubaneswarensis and Thiobacillus novellus.
Gut inflammation provides a respiratory electron acceptor for Salmonella, and thiosulfate respiration supports its expansion.
CRISPR knockout, point-mutation, knock-in, and overexpression models can test the causal role of candidate transporters in thiosulfate flux and anion competition.
Radiolabeled flux assays, anion competition assays, bacterial genetics, RNA-seq, proteomics, and imaging are commonly used.
Yes, SLC13A1 is a Na+-sulfate cotransporter, and thiosulfate interacts with sulfate transport pathways in renal and epithelial systems.
Thiosulfate transport has been linked to calcium oxalate nephrolithiasis, gut inflammation and Salmonella infection, and bacterial sulfur metabolism.

Conclusion

GO:0015709 thiosulfate transport is a biologically_process annotation that captures the directed movement of thiosulfate across membranes. It is experimentally grounded in bacterial bioenergetics, host-microbe interactions, and mammalian renal anion handling. Researchers can leverage CRISPR knockout, point-mutation, knock-in, and overexpression models to dissect the genes and mechanisms underlying thiosulfate transport. As a target for functional genomics, thiosulfate transport offers opportunities to connect sulfur metabolism to disease-relevant phenotypes such as kidney stone formation and infection. EDITGENE provides the cell models and screening services needed to advance this research.

References

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  2. 2. Markovich D. 2014. Na+-sulfate cotransporter SLC13A1.. Pflugers Arch 466(1):131-7 PMID: 24193406
  3. 3. Narayan KD et al.. 2017. Mechanism of electron transport during thiosulfate oxidation in an obligately mixotrophic bacterium Thiomonas bhubaneswarensis strain S10 (DSM 18181(T)).. Appl Microbiol Biotechnol 101(3):1239-1252 PMID: 27832308
  4. 4. Hicks JL et al.. 2018. Cysteine biosynthesis in Neisseria species.. Microbiology (Reading) 164(12):1471-1480 PMID: 30307392
  5. 5. Ullrich KJ et al.. 1980. Bidirectional active transport of thiosulfate in the proximal convolution of the rat kidney.. Pflugers Arch 387(2):127-32 PMID: 7191976
  6. 6. Aleem MI. 1965. Thiosulfate Oxidation and Electron Transport in Thiobacillus novellus.. J Bacteriol 90(1):95-101 PMID: 16562048
  7. 7. Winter SE et al.. 2010. Gut inflammation provides a respiratory electron acceptor for Salmonella.. Nature 467(7314):426-9 PMID: 20864996
  8. 8. Landry GM et al.. 2016. Sulfate and thiosulfate inhibit oxalate transport via a dPrestin (Slc26a6)-dependent mechanism in an insect model of calcium oxalate nephrolithiasis.. Am J Physiol Renal Physiol 310(2):F152-9 PMID: 26538444
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