GO:0015744 succinate transport: Mitochondrial and Cellular Transport Mechanisms, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0015744 succinate transport describes the directed movement of the succinate dianion across cellular membranes by transporters or pores.
• Succinate accumulation during ischaemia drives mitochondrial reactive oxygen species production and reperfusion injury, making succinate transport a therapeutic target.
• pH-gated succinate secretion regulates muscle remodeling in response to exercise, linking succinate transport to inter-organ metabolic signaling.
• Monocarboxylate transporters facilitate succinate uptake into brown adipocytes, identifying MCTs as succinate carriers.
• Succinate transport is conserved from bacteria such as Rhizobium and ruminal selenomonads to mammals.
• CRISPR knockout, knock-in, and overexpression models enable causal dissection of succinate transporter genes in disease and metabolism.
Description
Succinate is a central metabolite of the tricarboxylic acid cycle and a signaling molecule, and its movement across membranes is essential for cellular metabolism and inter-organ communication. GO:0015744 succinate transport is defined as the directed movement of the succinate dianion into, out of, or within a cell, or between cells, by means of a transporter or pore. This process is mediated by specific membrane proteins, including mitochondrial carriers and monocarboxylate transporters, and is conserved across prokaryotes and eukaryotes. Researchers study succinate transport because its dysregulation contributes to ischaemia-reperfusion injury, metabolic disease, and host-pathogen interactions. Understanding the genes and mechanisms of succinate transport provides a foundation for therapeutic targeting and metabolic engineering.
succinate transport At A Glance
| GO ID | GO:0015744 |
|---|---|
| GO term | succinate transport |
| Ontology | biological_process |
| Synonym | none |
| Major function | Directed movement of succinate dianion across membranes by transporters or pores |
| Definition source | QuickGO |
| Related molecules | Succinate, mitochondrial carriers, monocarboxylate transporters |
| Cellular locations | Mitochondrial inner membrane, plasma membrane, bacterial membranes |
| Disease relevance | Ischaemia-reperfusion injury, metabolic signaling, host-pathogen interactions |
What Is GO:0015744?
GO:0015744 succinate transport is the biological process in which the succinate dianion, the ionized form of ethane dicarboxylic acid, is moved across a membrane or within a cell by a transporter or pore. This process can occur into, out of, or between cells and is distinct from succinate metabolism or signaling.
Why Is succinate transport Important in Cell Biology?
Succinate transport is critical because succinate accumulation during ischaemia drives mitochondrial reactive oxygen species production and tissue damage upon reperfusion, and pH-gated succinate secretion regulates muscle remodeling after exercise. In brown adipocytes, succinate uptake via monocarboxylate transporters supports thermogenesis, while in tuberculosis, succinate transport contributes to pathogenic mitochondrial ROS. These findings position succinate transport as a target for cardioprotection, metabolic modulation, and anti-infective strategies.
• Succinate accumulation during ischaemia drives reperfusion injury through mitochondrial ROS.
• Mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury.
• pH-gated succinate secretion regulates muscle remodeling in response to exercise.
• Monocarboxylate transporters facilitate succinate uptake into brown adipocytes.
• Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport involving succinate.
• Succinate transport is conserved in bacteria such as Rhizobium japonicum and Rhizobium leguminosarum.
• Ruminal selenomonads regulate succinate transport by carbohydrate availability and osmotic strength.
• Succinate transport links metabolism to inter-organ signaling and immune responses.
• Targeting succinate transport may reduce ischaemia-reperfusion injury in heart and other organs.
• CRISPR models enable functional dissection of succinate transporter genes in disease.
What Happens During succinate transport?
Succinate accumulation and mitochondrial transport
In simple terms: During ischaemia, succinate builds up in mitochondria and is transported across the inner membrane.
Ischaemic accumulation of succinate occurs in mitochondria and controls reperfusion injury through mitochondrial ROS. Mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury, indicating that specific carriers move succinate across the inner membrane.
pH-gated succinate secretion
In simple terms: Cells can release succinate depending on pH, which acts as a signal for muscle remodeling.
pH-gated succinate secretion regulates muscle remodeling in response to exercise, demonstrating that succinate export is a regulated process.
Succinate uptake by monocarboxylate transporters
In simple terms: Certain transporters take succinate into cells such as brown adipocytes.
Monocarboxylate transporters facilitate succinate uptake into brown adipocytes, identifying a specific route for succinate entry.
Bacterial succinate transport
In simple terms: Bacteria also take up succinate using dedicated transport systems.
Succinate transport by free-living forms of Rhizobium japonicum and Rhizobium leguminosarum has been characterized, showing conserved mechanisms. Ruminal selenomonads regulate succinate transport by carbohydrate availability and osmotic strength.
Succinate transport in host-pathogen interactions
In simple terms: Succinate transport can influence immune responses during infection.
Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport, a process linked to succinate transport.
Key Genes Involved in GO:0015744 succinate transport
The following genes and proteins are involved in succinate transport across different organisms and cellular contexts.
| Gene | Major Role | Research Relevance |
|---|---|---|
| SLC25A10 | Mitochondrial dicarboxylate carrier | Succinate transport across inner membrane |
| SLC25A11 | Mitochondrial oxoglutarate carrier | May transport succinate in mitochondria |
| MCT1 (SLC16A1) | Monocarboxylate transporter | Succinate uptake in brown adipocytes |
| MCT4 (SLC16A3) | Monocarboxylate transporter | Succinate transport in muscle |
| SDHA | Succinate dehydrogenase subunit | Succinate oxidation and accumulation |
| SDHB | Succinate dehydrogenase subunit | Succinate metabolism and transport |
| SDHC | Succinate dehydrogenase subunit | Succinate oxidation |
| SDHD | Succinate dehydrogenase subunit | Succinate metabolism |
| Rhizobium japonicum succinate transporter | Bacterial succinate uptake | Free-living forms |
| Rhizobium leguminosarum succinate transporter | Bacterial succinate uptake | Symbiotic nitrogen fixation |
| Ruminal selenomonad succinate transporter | Succinate transport regulation | Carbohydrate availability and osmotic strength |
| TNF | Cytokine inducing mitochondrial ROS | Tuberculosis pathogenesis |
| Mitochondrial carriers (general) | Succinate transport across inner membrane | Ischaemia-reperfusion injury |
| Monocarboxylate transporters (general) | Succinate uptake and secretion | Exercise and thermogenesis |
| Succinate dehydrogenase complex | Succinate oxidation | Reperfusion injury |
| Reverse electron transport chain components | ROS production | Tuberculosis |
How Is succinate transport Regulated?
Succinate transport is regulated by pH, as pH-gated succinate secretion controls muscle remodeling in response to exercise. In ruminal selenomonads, succinate transport is regulated by carbohydrate availability and osmotic strength. Mitochondrial succinate transport is required for ischaemia/reperfusion injury, suggesting regulation by ischaemic conditions.
succinate transport and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SLC25A10 | Cardiac ischaemia/reperfusion injury | Knockout mouse |
| MCT1 (SLC16A1) | Brown adipocyte thermogenesis | Knockout cell line |
| MCT4 (SLC16A3) | Muscle remodeling | Knockout mouse |
| SDHA | Reperfusion injury | Point mutation knock-in |
| TNF | Tuberculosis | Knockout macrophage |
Ischaemia-reperfusion injury
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS, and mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury. Targeting succinate transport may reduce tissue damage after myocardial infarction.
Metabolic and exercise physiology
pH-gated succinate secretion regulates muscle remodeling in response to exercise, linking succinate transport to metabolic adaptation. Monocarboxylate transporters facilitate succinate uptake into brown adipocytes, affecting thermogenesis.
Infectious disease
Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport, a process involving succinate transport.
From succinate transport-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does SLC25A10 mediate mitochondrial succinate transport? | Knockout cell line |
| Does MCT1 facilitate succinate uptake in brown adipocytes? | Knockout adipocytes |
| Does pH-gated succinate secretion regulate muscle remodeling? | Knock-in reporter mouse |
| Does succinate accumulation drive reperfusion injury? | Point mutation knock-in mouse |
| Does TNF-induced ROS require succinate transport? | Knockout macrophages |
| Can bacterial succinate transport be engineered? | Overexpression in Rhizobium |
How to Study the succinate transport Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Metabolic flux analysis | Succinate transport rate | Mitochondrial transport |
| Genetically encoded sensors | Intracellular succinate levels | Live-cell imaging |
| CRISPR knockout screening | Genes required for succinate transport | Transporter discovery |
| Proteomics | Transporter protein interactions | Complex identification |
| RNA-seq | Expression of transporter genes | Regulation studies |
| Seahorse assay | Mitochondrial respiration | Reperfusion injury |
| Bacterial growth assays | Succinate uptake | Microbial transport |
Metabolic flux analysis
Metabolic flux analysis using labeled succinate can measure transport rates in cells and mitochondria.
Genetically encoded sensors
Genetically encoded succinate sensors enable real-time monitoring of succinate transport in live cells.
CRISPR screening
CRISPR knockout screens can identify genes required for succinate transport and accumulation.
Proteomics and interactomics
Proteomics can identify transporter complexes and post-translational modifications regulating succinate transport.
How CRISPR Can Be Used to Study GO:0015744 succinate transport
Knockout
CRISPR knockout of SLC25A10 or MCT1 can abolish succinate transport, revealing its role in ischaemia-reperfusion injury and thermogenesis.
Point Mutation
Point mutations in succinate transporter genes can dissect residues required for substrate binding and pH gating.
Knock-in
Knock-in of tagged transporters enables localization and interaction studies in native tissues.
Overexpression
Overexpression of succinate transporters can enhance succinate uptake and drive metabolic remodeling.
How EDITGENE Supports succinate transport Research
Researchers studying succinate transport-related genes often need to determine whether a candidate gene is causally involved in succinate movement, metabolic signaling, or disease. EDITGENE provides CRISPR-based cell models and screening services to accelerate this research.
Contact EDITGENE today to design your custom CRISPR model for succinate transport research.
Frequently Asked Questions About succinate transport
What is succinate transport?
Succinate transport is the directed movement of the succinate dianion across membranes by transporters or pores, defined as GO:0015744.
What genes are involved in succinate transport?
Genes include SLC25A10, SLC25A11, MCT1 (SLC16A1), MCT4 (SLC16A3), and SDH subunits, as well as bacterial transporters.
Why is succinate transport important in ischaemia?
Succinate accumulation during ischaemia drives mitochondrial ROS and reperfusion injury, and mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury.
How is succinate transport regulated?
It is regulated by pH, carbohydrate availability, and osmotic strength, as shown in muscle and ruminal bacteria.
What diseases are linked to succinate transport?
Ischaemia-reperfusion injury, metabolic disorders, and tuberculosis are linked to succinate transport.
What methods study succinate transport?
Metabolic flux analysis, genetically encoded sensors, CRISPR screening, and proteomics are commonly used.
Can CRISPR knockout help study succinate transport?
Yes, CRISPR knockout of transporter genes such as SLC25A10 or MCT1 can abolish succinate transport and reveal its function.
Is succinate transport conserved in bacteria?
Yes, succinate transport has been characterized in Rhizobium japonicum, Rhizobium leguminosarum, and ruminal selenomonads.
What is the role of monocarboxylate transporters in succinate transport?
Monocarboxylate transporters facilitate succinate uptake into brown adipocytes.
How does succinate transport affect exercise?
pH-gated succinate secretion regulates muscle remodeling in response to exercise.
Conclusion
GO:0015744 succinate transport is a fundamental biological process with critical roles in ischaemia-reperfusion injury, metabolic signaling, and host-pathogen interactions. The identification of specific transporters such as SLC25A10 and MCT1 provides targets for therapeutic intervention and metabolic engineering. Continued research using CRISPR models and advanced screening will further elucidate the regulation and disease relevance of succinate transport.
References
- 1. Chouchani ET et al.. 2014. Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.. Nature 515(7527):431-435 PMID: 25383517
- 2. Reddy A et al.. 2020. pH-Gated Succinate Secretion Regulates Muscle Remodeling in Response to Exercise.. Cell 183(1):62-75.e17 PMID: 32946811
- 3. Pala L et al.. 2026. Mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury.. Cardiovasc Res 122(6):734-747 PMID: 41603375
- 4. Reddy A et al.. 2024. Monocarboxylate transporters facilitate succinate uptake into brown adipocytes.. Nat Metab 6(3):567-577 PMID: 38378996
- 5. Roca FJ et al.. 2022. Tumor necrosis factor induces pathogenic mitochondrial ROS in tuberculosis through reverse electron transport.. Science 376(6600):eabh2841 PMID: 35737799
- 6. McAllister CF et al.. 1983. Succinate transport by free-living forms of Rhizobium japonicum.. J Bacteriol 153(3):1155-62 PMID: 6402487
- 7. Finan TM et al.. 1981. Succinate transport in Rhizobium leguminosarum.. J Bacteriol 148(1):193-202 PMID: 7287623
- 8. Strobel HJ et al.. 1991. Succinate transport by a ruminal selenomonad and its regulation by carbohydrate availability and osmotic strength.. Appl Environ Microbiol 57(1):248-54 PMID: 2036012
