GO:0015910 long-chain fatty acid import into peroxisome: Peroxisomal Fatty Acid Transport Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0015910 describes the directed movement of long-chain fatty acids (13-22 carbons) into the peroxisome, a process essential for peroxisomal beta-oxidation and lipid biosynthesis.
• The peroxisomal ABC transporter ABCD1 (ALDP) is the principal protein implicated in long-chain fatty acid import, and its dysfunction causes X-linked adrenoleukodystrophy (X-ALD).
• ABCD3 (PMP70) is a closely related peroxisomal ABC transporter that also contributes to fatty acid transport, with recent structural studies revealing its substrate transport mechanism.
• Long-chain fatty acid import supports de novo ether lipid/plasmalogen synthesis, and the origin of these fatty acids has been traced to peroxisomal import pathways.
• Defects in peroxisomal fatty acid import are linked to neurodegeneration, aging-related intestinal stem cell dysfunction, and cancer metabolic reprogramming.
• CRISPR-based knockout, knock-in, and overexpression models are powerful tools for dissecting the causal roles of ABCD1, ABCD3, and related genes in peroxisomal fatty acid import.
Description
Long-chain fatty acid import into peroxisome (GO:0015910) is a biological process defined as the directed movement of a long-chain fatty acid, an aliphatic molecule containing 13 to 22 carbons, into a peroxisome. Peroxisomes are ubiquitous organelles that perform essential metabolic functions, including beta-oxidation of very long-chain fatty acids, synthesis of ether lipids and plasmalogens, and detoxification of reactive oxygen species. The import of long-chain fatty acids into peroxisomes is a prerequisite for these processes, and its disruption has profound consequences for cellular lipid homeostasis and human health. The peroxisomal membrane forms a selective barrier, and dedicated transport proteins are required to translocate long-chain fatty acids from the cytosol into the peroxisomal matrix. The ATP-binding cassette (ABC) transporters ABCD1 and ABCD3 are the best-characterized proteins involved in this process, and mutations in ABCD1 cause X-linked adrenoleukodystrophy (X-ALD), a severe neurodegenerative disorder characterized by accumulation of very long-chain fatty acids in plasma and tissues. Recent structural and biochemical studies have begun to elucidate the molecular mechanism by which ABCD3 recognizes and transports fatty acid substrates. Beyond X-ALD, peroxisomal long-chain fatty acid import has been implicated in diverse physiological and pathological contexts, including aging-related intestinal stem cell differentiation, maternal obesity-induced epigenetic reprogramming, and hepatocellular carcinoma progression. Understanding the genes, mechanisms, and regulation of GO:0015910 is therefore critical for researchers in neurobiology, metabolism, cancer biology, and developmental biology. This article provides a comprehensive overview of the process, its key genes, disease relevance, and the CRISPR-based research methods available to study it.
long-chain fatty acid import into peroxisome At A Glance
| GO ID | GO:0015910 |
|---|---|
| GO term | long-chain fatty acid import into peroxisome |
| Ontology | biological_process |
| Synonym | peroxisomal long-chain fatty acid import; peroxisomal long-chain fatty acid uptake |
| Definition | The directed movement of a long-chain fatty acid into a peroxisome. A long-chain fatty acid has an aliphatic tail containing 13 to 22 carbons. |
| Major function | Supplies long-chain fatty acids for peroxisomal beta-oxidation and ether lipid/plasmalogen biosynthesis. |
| Key transporters | ABCD1 (ALDP), ABCD3 (PMP70). |
| Associated diseases | X-linked adrenoleukodystrophy, aging-related intestinal dysfunction, hepatocellular carcinoma. |
| Research methods | CRISPR knockout/knock-in, lipidomics, transport assays, structural biology. |
What Is GO:0015910?
GO:0015910, long-chain fatty acid import into peroxisome, is the directed movement of a long-chain fatty acid (a fatty acid with an aliphatic tail of 13 to 22 carbons) into a peroxisome. This process is synonymous with peroxisomal long-chain fatty acid import and peroxisomal long-chain fatty acid uptake. It is a biological process that enables peroxisomes to acquire the fatty acid substrates necessary for beta-oxidation, ether lipid synthesis, and other metabolic pathways.
Why Is long-chain fatty acid import into peroxisome Important in Cell Biology?
Long-chain fatty acid import into peroxisomes is essential for cellular lipid metabolism, and its dysfunction is directly linked to severe human diseases. The peroxisomal ABC transporter ABCD1 is the causative gene for X-linked adrenoleukodystrophy, a devastating neurodegenerative disease characterized by the accumulation of very long-chain fatty acids due to impaired peroxisomal beta-oxidation. Beyond X-ALD, peroxisomal long-chain fatty acid import has been implicated in aging-related intestinal stem cell differentiation through very long-chain fatty acid oxidation, in maternal obesity-induced epigenetic reprogramming during zygotic genome activation, and in hepatocellular carcinoma as a pro-tumorigenic metabolic adaptation. Understanding the molecular mechanism of this process, including the role of ABCD3 and other transporters, is therefore of broad biomedical importance.
• Provides long-chain fatty acids for peroxisomal beta-oxidation, a pathway essential for lipid homeostasis.
• Supports de novo ether lipid and plasmalogen synthesis, which are critical for membrane integrity and signaling.
• Dysfunction of ABCD1 causes X-linked adrenoleukodystrophy, a severe neurodegenerative disorder.
• Implicated in aging-related intestinal stem cell differentiation through very long-chain fatty acid oxidation.
• Linked to maternal obesity-induced epigenetic reprogramming during zygotic genome activation.
• Plays a role in hepatocellular carcinoma progression as a pro-tumorigenic metabolic adaptation.
• ABCD3 structure-function studies provide mechanistic insights into substrate transport.
• Peroxisome biogenesis disorders affect multiple organs and highlight the importance of peroxisomal import.
• CRISPR-based models enable causal testing of genes involved in this process.
• Potential therapeutic target for metabolic and neurodegenerative diseases.
What Happens During long-chain fatty acid import into peroxisome?
Recognition and Binding of Long-Chain Fatty Acids at the Peroxisomal Membrane
In simple terms: The peroxisome must first grab long-chain fatty acids from the cytosol before they can be moved inside.
The initial step of long-chain fatty acid import into peroxisomes involves the recognition and binding of long-chain fatty acids (13-22 carbons) at the cytosolic face of the peroxisomal membrane. The peroxisomal ABC transporter ABCD1 (ALDP) is a key protein involved in this process, and mutations in ABCD1 impair the transport of very long-chain fatty acids into peroxisomes, leading to their accumulation in X-linked adrenoleukodystrophy. ABCD3 (PMP70), another peroxisomal ABC transporter, also contributes to fatty acid transport, and recent structural studies have revealed the molecular basis of substrate recognition and transport by human ABCD3. The peroxisomal membrane itself is a selective barrier that requires dedicated transport proteins for fatty acid translocation.
Translocation Across the Peroxisomal Membrane
In simple terms: Once bound, the fatty acid is moved across the peroxisomal membrane into the organelle interior.
Following recognition, long-chain fatty acids are translocated across the peroxisomal membrane. The ABC transporters ABCD1 and ABCD3 are thought to function as homodimers or heterodimers that utilize ATP hydrolysis to drive substrate transport. The molecular mechanism of substrate transport by human peroxisomal ABCD3 has been elucidated through structural and biochemical studies, revealing conformational changes that facilitate fatty acid movement across the membrane. This translocation step is rate-limiting for peroxisomal beta-oxidation, as the fatty acids must be delivered to the peroxisomal matrix where beta-oxidation enzymes reside.
Delivery to Peroxisomal Beta-Oxidation Machinery
In simple terms: Inside the peroxisome, the imported fatty acids are handed off to enzymes that break them down.
After translocation into the peroxisome, long-chain fatty acids are delivered to the peroxisomal beta-oxidation machinery. Peroxisomal beta-oxidation is responsible for the chain shortening of very long-chain fatty acids, and the imported long-chain fatty acids serve as substrates for this process. The oxidation of very long-chain fatty acids in peroxisomes is critical for cellular lipid homeostasis, and its disruption leads to the accumulation of toxic fatty acid species. Aging-related peroxisomal dysregulation disrupts intestinal stem cell differentiation through alterations of very long-chain fatty acid oxidation, highlighting the importance of this delivery step.
Contribution to Ether Lipid and Plasmalogen Synthesis
In simple terms: Imported fatty acids are also used as building blocks for specialized membrane lipids.
Long-chain fatty acids imported into peroxisomes are not only oxidized but also serve as substrates for de novo ether lipid and plasmalogen synthesis. The origin of long-chain fatty acids required for de novo ether lipid/plasmalogen synthesis has been investigated, and peroxisomal import pathways are a major source. Ether lipids and plasmalogens are essential components of cell membranes, and their synthesis depends on the availability of long-chain fatty acids within peroxisomes. This biosynthetic role underscores the dual importance of GO:0015910 in both catabolic and anabolic lipid pathways.
Regulation of Long-Chain Fatty Acid Import
In simple terms: The cell adjusts how much fatty acid enters peroxisomes based on its metabolic needs.
The import of long-chain fatty acids into peroxisomes is subject to regulation at multiple levels. Peroxisome biogenesis and the expression of peroxisomal transporters are regulated by transcription factors such as PPARalpha, although the specific regulatory mechanisms for GO:0015910 are still being elucidated. Maternal obesity disrupts epigenetic reprogramming via peroxisomal-dependent phospholipid-methyl uncoupling during zygotic genome activation, suggesting that peroxisomal fatty acid import is sensitive to maternal metabolic state. Additionally, SLC27A5 deficiency-induced reduction in long-chain fatty acid uptake in hepatocellular carcinoma indicates that fatty acid transport pathways can be rewired in cancer.
Key Genes Involved in GO:0015910 long-chain fatty acid import into peroxisome
The following genes and proteins are the principal molecular players in long-chain fatty acid import into peroxisomes (GO:0015910) and related peroxisomal lipid metabolism.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ABCD1 | Peroxisomal ABC transporter (ALDP) that imports very long-chain fatty acids into peroxisomes; mutations cause X-ALD. | Primary disease gene for X-linked adrenoleukodystrophy; target for gene therapy and knockout studies. |
| ABCD3 | Peroxisomal ABC transporter (PMP70) involved in fatty acid transport; structural studies reveal substrate transport mechanism. | Mechanistic studies of peroxisomal fatty acid import; potential modifier of X-ALD. |
| SLC27A5 | Fatty acid transport protein; deficiency reduces long-chain fatty acid uptake in hepatocellular carcinoma. | Cancer metabolism; pro-tumorigenic adaptation and glutaminase inhibitor sensitivity. |
| PEX genes (e.g., PEX1, PEX6) | Peroxisome biogenesis factors required for peroxisome formation and import machinery. | Peroxisome biogenesis disorders; models for studying import defects. |
| ACOX1 | Peroxisomal acyl-CoA oxidase that catalyzes the first step of beta-oxidation. | Beta-oxidation studies; links import to oxidation. |
| HSD17B4 | Peroxisomal multifunctional enzyme involved in beta-oxidation. | Lipid metabolism research. |
| SCPx | Peroxisomal thiolase involved in beta-oxidation. | Beta-oxidation pathway analysis. |
| GNPAT | Dihydroxyacetone phosphate acyltransferase involved in ether lipid synthesis. | Ether lipid/plasmalogen synthesis studies. |
| AGPS | Alkylglycerone phosphate synthase involved in ether lipid synthesis. | Plasmalogen biosynthesis research. |
| FAR1 | Fatty acyl-CoA reductase involved in ether lipid synthesis. | Lipid biosynthesis studies. |
| PPARA | Transcription factor regulating peroxisomal gene expression. | Regulation of peroxisomal import and beta-oxidation. |
| SLC25A17 | Peroxisomal membrane carrier for cofactors. | Peroxisomal transport studies. |
| PMP70 | Alternative name for ABCD3; peroxisomal membrane protein. | Structural and functional studies. |
| ALDP | Alternative name for ABCD1; adrenoleukodystrophy protein. | X-ALD diagnostics and modeling. |
| VLCFA-CoA synthetase | Activates very long-chain fatty acids for peroxisomal import. | Enzyme assays for import. |
| Catalase | Peroxisomal enzyme that detoxifies hydrogen peroxide. | Peroxisomal marker and functional studies. |
How Is long-chain fatty acid import into peroxisome Regulated?
The import of long-chain fatty acids into peroxisomes is regulated at the transcriptional and post-transcriptional levels. Peroxisome biogenesis and the expression of peroxisomal transporters such as ABCD1 and ABCD3 are controlled by nuclear receptors including PPARalpha, which responds to lipid availability. Maternal obesity has been shown to disrupt epigenetic reprogramming via peroxisomal-dependent phospholipid-methyl uncoupling during zygotic genome activation, indicating that peroxisomal fatty acid import is sensitive to maternal metabolic status. In hepatocellular carcinoma, SLC27A5 deficiency reduces long-chain fatty acid uptake, representing a metabolic adaptation that can be targeted by glutaminase inhibition. These findings suggest that GO:0015910 is dynamically regulated in response to developmental, metabolic, and pathological cues.
long-chain fatty acid import into peroxisome and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ABCD1 | X-linked adrenoleukodystrophy; impaired VLCFA import | ABCD1 knockout cell lines and mouse models; patient-derived fibroblasts |
| ABCD3 | Peroxisomal fatty acid transport; potential modifier of X-ALD | ABCD3 knockout and knock-in models; structural studies |
| SLC27A5 | Hepatocellular carcinoma; reduced long-chain fatty acid uptake | SLC27A5 knockout HCC cell lines; glutaminase inhibitor sensitivity assays |
| PEX genes | Peroxisome biogenesis disorders | PEX knockout models; peroxisomal import assays |
| GNPAT/AGPS | Ether lipid/plasmalogen synthesis defects | Knockout models for lipidomics and plasmalogen analysis |
X-linked Adrenoleukodystrophy (X-ALD)
X-linked adrenoleukodystrophy is a severe neurodegenerative disorder caused by mutations in the ABCD1 gene, which encodes the peroxisomal ABC transporter ALDP. Loss of ABCD1 function impairs the import of very long-chain fatty acids into peroxisomes, leading to their accumulation in plasma and tissues, which is the biochemical hallmark of the disease. The ABCD1 mutation database has been instrumental in establishing genotype-phenotype correlations and in diagnosing X-ALD. Clinical manifestations include progressive demyelination, adrenal insufficiency, and neurological decline, with varying severity depending on the mutation and other genetic modifiers.
Aging-related Intestinal Stem Cell Dysfunction
Aging-related peroxisomal dysregulation disrupts intestinal stem cell differentiation through alterations of very long-chain fatty acid oxidation. This study links peroxisomal fatty acid import and oxidation to the maintenance of intestinal stem cell function during aging, suggesting that GO:0015910 plays a role in tissue homeostasis and regenerative capacity. The findings highlight the importance of peroxisomal lipid metabolism in age-related physiological decline.
Hepatocellular Carcinoma
SLC27A5 deficiency-induced reduction in long-chain fatty acid uptake is a pro-tumorigenic metabolic adaptation and confers sensitivity to glutaminase inhibition in hepatocellular carcinoma. This study demonstrates that alterations in long-chain fatty acid transport, which may involve peroxisomal import pathways, can reprogram cancer cell metabolism and create therapeutic vulnerabilities. The link between GO:0015910 and cancer metabolism is an emerging area of research.
Maternal Obesity and Epigenetic Reprogramming
Maternal obesity disrupts epigenetic reprogramming via peroxisomal-dependent phospholipid-methyl uncoupling during zygotic genome activation. This finding implicates peroxisomal fatty acid import and metabolism in early embryonic development and suggests that maternal metabolic status can affect offspring through peroxisomal pathways. The study provides evidence that GO:0015910 is important beyond adult physiology.
From long-chain fatty acid import into peroxisome-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does ABCD1 loss impair long-chain fatty acid import? | ABCD1 knockout cell line (e.g., HeLa, fibroblasts) |
| What is the substrate specificity of ABCD3? | ABCD3 point-mutation knock-in models and transport assays |
| Can restored ABCD1 expression rescue X-ALD phenotypes? | ABCD1 knock-in or overexpression in patient-derived cells |
| How does SLC27A5 deficiency affect cancer metabolism? | SLC27A5 knockout hepatocellular carcinoma cells |
| What is the role of peroxisomal import in aging? | Aging mouse models with peroxisomal gene knockouts |
| How does maternal obesity affect peroxisomal import? | Maternal obesity mouse models and zygotic genome activation assays |
How to Study the long-chain fatty acid import into peroxisome Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Lipidomics | Quantification of long-chain and very long-chain fatty acids | Diagnosis of X-ALD; assessing import defects |
| Transport assays | Rate of fatty acid import into peroxisomes | Functional characterization of ABCD1/ABCD3 |
| Cryo-EM/X-ray crystallography | Three-dimensional structure of transporters | Mechanistic studies of ABCD3 |
| CRISPR knockout screens | Identification of genes regulating import | Discovery of novel regulators |
| Fluorescence microscopy | Peroxisome morphology and protein localization | Visualizing import dynamics |
| RNA-seq | Transcriptional changes in peroxisomal genes | Regulation studies |
| Proteomics | Protein composition of peroxisomes | Identifying import machinery components |
| Metabolic flux analysis | Flux through beta-oxidation pathways | Assessing metabolic consequences |
Lipidomics and Fatty Acid Profiling
Lipidomics and fatty acid profiling are essential for measuring the import and metabolism of long-chain fatty acids in peroxisomes. These methods can quantify very long-chain fatty acid accumulation in ABCD1-deficient cells, a hallmark of X-ALD. They are also used to assess the impact of SLC27A5 deficiency on long-chain fatty acid uptake in hepatocellular carcinoma and to study ether lipid/plasmalogen synthesis.
Transport Assays and Structural Biology
Transport assays using isolated peroxisomes or reconstituted systems can directly measure long-chain fatty acid import activity. Structural biology approaches, such as cryo-EM and X-ray crystallography, have been used to elucidate the molecular mechanism of substrate transport by human peroxisomal ABCD3. These methods provide mechanistic insights into how mutations in ABCD1 and ABCD3 affect transport function.
CRISPR-based Genetic Screens
CRISPR knockout and activation screens can identify genes that regulate long-chain fatty acid import into peroxisomes. For example, screens in cancer cell lines have revealed metabolic vulnerabilities linked to fatty acid transport. These screens are powerful for discovering novel regulators of GO:0015910 and for validating candidate genes.
Imaging and Peroxisome Tracking
Fluorescence microscopy with peroxisome-targeted reporters can visualize peroxisomal dynamics and fatty acid import in live cells. Imaging studies have been used to study peroxisome biogenesis and the localization of ABCD1 and ABCD3. These methods complement biochemical assays and provide spatial information about the import process.
How CRISPR Can Be Used to Study GO:0015910 long-chain fatty acid import into peroxisome
Knockout
CRISPR knockout of ABCD1 or ABCD3 in cell lines can abolish long-chain fatty acid import, leading to accumulation of very long-chain fatty acids and providing a model for X-ALD. Knockout of SLC27A5 in hepatocellular carcinoma cells reduces long-chain fatty acid uptake and confers sensitivity to glutaminase inhibition. These models are valuable for studying the loss-of-function consequences of GO:0015910 genes.
Point Mutation
CRISPR point mutation can introduce specific disease-associated mutations in ABCD1, such as those found in X-ALD patients, to study genotype-phenotype correlations. Point mutations in ABCD3 can be used to dissect the substrate transport mechanism and identify residues critical for fatty acid recognition. These models allow precise testing of mutation effects on import activity.
Knock-in
CRISPR knock-in can be used to tag endogenous ABCD1 or ABCD3 with fluorescent or affinity tags for localization and interaction studies. Knock-in of wild-type ABCD1 into patient-derived cells can rescue the import defect and serve as a proof-of-concept for gene therapy. These models are essential for understanding the dynamic behavior of peroxisomal transporters.
Overexpression
CRISPR activation or cDNA overexpression can increase the levels of ABCD1, ABCD3, or SLC27A5 to study their effects on long-chain fatty acid import and downstream metabolism. Overexpression of ABCD1 in X-ALD cells can restore peroxisomal beta-oxidation and reduce very long-chain fatty acid accumulation. These models help identify rate-limiting steps and potential therapeutic targets.
How EDITGENE Supports long-chain fatty acid import into peroxisome Research
Researchers studying long-chain fatty acid import into peroxisome-related genes often need to determine whether a candidate gene is causally involved in the transport process, how specific mutations affect protein function, and whether restoring gene activity can rescue disease phenotypes. EDITGENE provides a comprehensive suite of CRISPR-based services to address these questions with precision and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for long-chain fatty acid import into peroxisome research.
Frequently Asked Questions About long-chain fatty acid import into peroxisome
What is long-chain fatty acid import into peroxisome (GO:0015910)?
GO:0015910 is the biological process of directed movement of long-chain fatty acids (13-22 carbons) into a peroxisome, which is essential for peroxisomal beta-oxidation and ether lipid synthesis.
What genes are involved in long-chain fatty acid import into peroxisome?
Key genes include ABCD1, ABCD3, SLC27A5, and peroxisome biogenesis genes such as PEX1 and PEX6.
Which transporter is responsible for peroxisomal long-chain fatty acid import?
The peroxisomal ABC transporters ABCD1 (ALDP) and ABCD3 (PMP70) are the primary transporters mediating long-chain fatty acid import.
What diseases are associated with defects in peroxisomal fatty acid import?
X-linked adrenoleukodystrophy is the most prominent disease, caused by ABCD1 mutations; other associations include aging-related intestinal dysfunction and hepatocellular carcinoma.
How is long-chain fatty acid import into peroxisomes studied?
Common methods include lipidomics, transport assays, structural biology (cryo-EM), CRISPR screens, and fluorescence microscopy.
What is the role of ABCD1 in X-linked adrenoleukodystrophy?
ABCD1 mutations impair the import of very long-chain fatty acids into peroxisomes, leading to their accumulation and causing neurodegeneration.
Can CRISPR be used to model peroxisomal fatty acid import defects?
Yes, CRISPR knockout of ABCD1 or ABCD3 in cell lines recapitulates import defects and provides models for studying disease mechanisms and potential therapies.
What is the relationship between peroxisomal fatty acid import and ether lipid synthesis?
Imported long-chain fatty acids are used as substrates for de novo ether lipid and plasmalogen synthesis within peroxisomes.
How does maternal obesity affect peroxisomal fatty acid import?
Maternal obesity disrupts epigenetic reprogramming via peroxisomal-dependent phospholipid-methyl uncoupling during zygotic genome activation, implicating peroxisomal import in developmental programming.
What is the clinical significance of very long-chain fatty acid accumulation?
Accumulation of very long-chain fatty acids due to impaired peroxisomal import is a biochemical hallmark of X-ALD and contributes to neuroinflammation and demyelination.
Conclusion
Long-chain fatty acid import into peroxisome (GO:0015910) is a fundamental biological process that supplies peroxisomes with fatty acid substrates for beta-oxidation and lipid biosynthesis. Its dysfunction is directly linked to X-linked adrenoleukodystrophy and has emerging roles in aging, cancer, and developmental programming. The molecular mechanisms of transport, particularly by ABCD1 and ABCD3, are being elucidated through structural and functional studies. CRISPR-based models are indispensable for dissecting the causal roles of genes involved in this process and for developing therapeutic strategies. EDITGENE offers a comprehensive portfolio of knockout, point mutation, knock-in, overexpression, and screening services to support researchers in advancing our understanding of GO:0015910 and its disease implications.
References
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- 5. Zhang XG et al.. 2026. Maternal obesity disrupts epigenetic reprogramming via peroxisomal-dependent phospholipid-methyl uncoupling during zygotic genome activation.. Nat Commun 17(1) PMID: 41851092
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