GO:0016559 peroxisome fission: Organelle Dynamics, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0016559 (peroxisome fission) is the biological process by which a mature peroxisome divides to form two or more separate peroxisome compartments.
• Peroxisome fission is driven by dynamin-related proteins and tail-anchored membrane adaptors, including MFF, which is a critical regulator of peroxisome maturation and division.
• Defects in peroxisome dynamics cause peroxisome biogenesis disorders and related neurological disease, reviewed as disorders of peroxisome dynamics.
• Peroxisome fission is metabolically coupled to mitochondrial function and thermogenesis, with peroxisome-derived lipids regulating cold-induced mitochondrial fission in adipose tissue.
• Mitochondrial and peroxisomal fission share molecular machinery and are relevant to cancer metabolism, kidney energetics, and aging muscle.
• CRISPR knockout, point-mutation, knock-in, and overexpression models are used to dissect the causal roles of fission genes such as MFF in peroxisome biology.
Description
Peroxisome fission (GO:0016559) is the division of a mature peroxisome within a cell to form two or more separate peroxisome compartments. Peroxisomes are single-membrane organelles that carry out essential oxidative reactions, and their number and size are maintained by a balance between de novo formation, growth, and division. Because peroxisomes cannot be made from scratch in all contexts, fission of existing organelles is a central route for propagating peroxisomal compartments during cell growth and division. The process is therefore fundamental to organelle homeostasis and to cellular metabolism. Researchers study peroxisome fission because its failure alters peroxisomal abundance and function, and because the machinery that executes fission is shared with mitochondrial dynamics. The tail-anchored protein MFF is a critical regulator of peroxisome maturation and division, linking peroxisomal and mitochondrial fission pathways. In addition, peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission, showing that peroxisome fission is metabolically integrated with whole-body energy balance. Consequently, GO:0016559 sits at the intersection of organelle biology, lipid metabolism, and disease, and it is a tractable target for CRISPR-based functional genomics.
peroxisome fission At A Glance
| GO ID | GO:0016559 |
|---|---|
| GO term | peroxisome fission |
| Ontology | biological_process |
| Definition | The division of a mature peroxisome within a cell to form two or more separate peroxisome compartments. |
| Synonyms | peroxisome division; peroxisome proliferation |
| Major function | Propagation and maintenance of peroxisomal compartments through division of mature peroxisomes. |
| Key machinery | Dynamin-related fission proteins and tail-anchored adaptors such as MFF. |
| Related process | Mitochondrial fission, with which peroxisome fission shares regulatory components. |
| Disease relevance | Disorders of peroxisome dynamics and peroxisome biogenesis disorders. |
What Is GO:0016559?
In plain terms, peroxisome fission is how one peroxisome splits into two or more peroxisomes. Formally, GO:0016559 describes the division of a mature peroxisome within a cell to form two or more separate peroxisome compartments. It is a biological process, and it is also known by the synonyms peroxisome division and peroxisome proliferation. The process requires membrane remodeling and constriction of the peroxisomal membrane, and it depends on dedicated fission factors such as MFF. Because the definition is restricted to division of an existing mature peroxisome, it is distinct from de novo peroxisome formation and from peroxisome degradation.
Why Is peroxisome fission Important in Cell Biology?
Peroxisome fission matters because it controls how many functional peroxisomes a cell has and therefore how much peroxisomal metabolism it can perform. When fission is impaired, peroxisomal compartments are not properly propagated, and this contributes to disorders of peroxisome dynamics that affect the nervous system and other organs. The process is also metabolically coupled to mitochondria: peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission, so peroxisome fission influences systemic energy expenditure. Because MFF is a critical regulator of peroxisome maturation and division, perturbations in fission machinery can simultaneously affect peroxisomal and mitochondrial dynamics. This dual role makes GO:0016559 important for understanding cancer metabolism, kidney energetics, and age-related muscle decline, where mitochondrial and peroxisomal fission are increasingly implicated.
• Maintains peroxisome number and size by dividing mature peroxisomes into separate compartments.
• Requires dedicated fission factors such as MFF, a critical regulator of peroxisome maturation and division.
• Is defective in disorders of peroxisome dynamics, which include neurological disease phenotypes.
• Couples peroxisomal lipid metabolism to cold-induced mitochondrial fission and adipose thermogenesis.
• Shares molecular components with mitochondrial fission, linking two major organelle dynamics pathways.
• Is relevant to cancer metabolism, where increased mitochondrial fission reprograms fatty acid metabolism.
• Contributes to kidney mitochondrial energetics, a process dependent on balanced organelle dynamics.
• Is implicated in aging muscle biology through mitochondrial dysfunction and sarcopenia pathways.
• Can be modulated by upstream regulators such as PGC-1alpha that control mitochondrial function.
• Provides a tractable target for CRISPR knockout, knock-in, and overexpression screens in organelle biology.
What Happens During peroxisome fission?
Initiation at the peroxisomal membrane
In simple terms: Fission starts when the peroxisome membrane is marked for division.
Peroxisome fission begins with the recruitment of fission machinery to the peroxisomal membrane. MFF is a critical regulator of peroxisome maturation and division, and its presence at the peroxisome is required for the organelle to divide properly. This initiation step is a prerequisite for the membrane remodeling that follows, and it distinguishes fission from de novo peroxisome formation.
Membrane constriction and division
In simple terms: The peroxisome membrane pinches inward until the organelle splits.
After initiation, the peroxisomal membrane undergoes constriction and division to generate two or more separate peroxisome compartments, which is the defining outcome of GO:0016559. This step depends on dynamin-related fission activity, and defects in the machinery produce abnormal peroxisome dynamics. Because the process produces separate compartments, it directly increases peroxisome number in the cell.
Coordination with mitochondrial fission
In simple terms: Peroxisome division is coordinated with the division of mitochondria.
Peroxisome fission is coordinated with mitochondrial fission because the two processes share components such as MFF. Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission, demonstrating that peroxisomal metabolism signals to mitochondrial dynamics. This coordination means that perturbations in peroxisome fission can have secondary effects on mitochondrial energetics.
Metabolic and thermogenic coupling
In simple terms: Peroxisome division is linked to how the body burns energy in fat tissue.
Peroxisome fission is metabolically coupled to thermogenesis, since peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission. This coupling places GO:0016559 within whole-body energy balance rather than only within cell-autonomous organelle biology. Upstream regulators of mitochondrial function, such as PGC-1alpha, provide a broader context in which organelle dynamics are controlled.
Failure of fission and disease
In simple terms: When fission fails, peroxisome dynamics become disordered and disease can follow.
Failure of peroxisome fission contributes to disorders of peroxisome dynamics, which are recognized causes of neurological and metabolic disease. Because fission is required to propagate functional peroxisomes, its impairment reduces the cell's capacity for peroxisomal metabolism. This is why genes such as MFF, a critical regulator of peroxisome maturation and division, are studied as disease-relevant factors.
Key Genes Involved in GO:0016559 peroxisome fission
The following genes and proteins are central to peroxisome fission (GO:0016559) and to the broader organelle dynamics machinery that supports it.
| Gene | Major Role | Research Relevance |
|---|---|---|
| MFF | Critical regulator of peroxisome maturation and division | Core fission factor for peroxisome and mitochondrial dynamics studies |
| DNM1L | Dynamin-related protein mediating membrane fission | Shared fission machinery for peroxisomes and mitochondria |
| PEX11B | Peroxisomal membrane protein involved in peroxisome division | Marker of peroxisome proliferation and fission |
| PEX11A | Peroxisomal membrane protein implicated in peroxisome division | Candidate for peroxisome abundance regulation |
| PEX11G | Peroxisomal membrane protein linked to peroxisome dynamics | Candidate for fission-related functional screens |
| FIS1 | Tail-anchored adaptor in organelle fission | Connects peroxisomal and mitochondrial fission pathways |
| MFF | Recruits fission machinery to peroxisomes | Target for knockout and knock-in studies |
| PGC-1A | Regulator of mitochondrial function and biogenesis | Upstream regulator of organelle dynamics |
| SIRT1 | Deacetylase linked to fatty acid metabolism reprogramming | Relevant to fission-driven metabolic changes |
| SIRT3 | Mitochondrial deacetylase in stress responses | Context for organelle dynamics and mitophagy |
| AMPK | Energy sensor kinase | Upstream regulator of organelle dynamics |
| PEX5 | Peroxisomal matrix protein import receptor | Peroxisome function context for fission studies |
| PEX1 | Peroxisome biogenesis ATPase | Peroxisome biogenesis disorder gene |
| PEX6 | Peroxisome biogenesis ATPase | Peroxisome biogenesis disorder gene |
| PEX26 | Peroxisomal membrane protein in biogenesis | Peroxisome biogenesis disorder gene |
| MFN2 | Mitochondrial fusion protein | Contrast to fission in organelle dynamics studies |
| OPA1 | Mitochondrial inner membrane fusion protein | Contrast to fission in organelle dynamics studies |
How Is peroxisome fission Regulated?
Peroxisome fission is regulated at the level of fission-factor recruitment and in coordination with mitochondrial dynamics. MFF is a critical regulator of peroxisome maturation and division, so changes in MFF abundance or localization directly modulate fission. Because peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission, cold and thermogenic stimuli can indirectly influence peroxisome-associated fission programs. Broader control of organelle dynamics is exerted by regulators of mitochondrial function such as PGC-1alpha, which coordinates mitochondrial biogenesis and function. Energy-sensing pathways involving AMPK and sirtuins provide additional context for how organelle dynamics are adjusted to metabolic state. In disease settings, dysregulation of these pathways is associated with altered fission and metabolic reprogramming.
peroxisome fission and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| MFF | Disorders of peroxisome dynamics | Knockout and knock-in cell models |
| DNM1L | Organelle fission defects | Point-mutation models of fission activity |
| PEX11B | Peroxisome proliferation defects | Overexpression and knockout models |
| SIRT1 | Hepatocellular carcinoma fatty acid metabolism | Knockout and overexpression in cancer cells |
| PGC-1A | Metabolic and mitochondrial dysfunction | Overexpression and knockout models |
Disorders of peroxisome dynamics
Disorders of peroxisome dynamics are a recognized group of diseases caused by defects in the machinery that controls peroxisome formation, division, and turnover. Because peroxisome fission is required to propagate functional peroxisomes, its impairment contributes to the cellular phenotypes seen in these disorders. MFF, a critical regulator of peroxisome maturation and division, is directly relevant to this disease category. These conditions frequently involve neurological and metabolic features, underscoring the importance of GO:0016559 for human health.
Metabolic and thermogenic disease
Peroxisome fission is linked to metabolic disease through its role in thermogenesis, since peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission. This connection means that altered peroxisome dynamics can influence energy expenditure and adipose function. Regulators of mitochondrial function such as PGC-1alpha provide a mechanistic framework for these effects. Consequently, GO:0016559 is relevant to obesity and metabolic syndrome research.
Cancer metabolism
Increased mitochondrial fission drives the reprogramming of fatty acid metabolism in hepatocellular carcinoma cells through suppression of Sirtuin 1, showing that fission dynamics are directly linked to cancer metabolism. Because peroxisome and mitochondrial fission share components such as MFF, peroxisome fission is part of the same organelle dynamics network that supports tumor metabolic reprogramming. This makes GO:0016559 a candidate process for studies of lipid metabolism in cancer.
Aging, kidney, and neurodegeneration
Mitochondrial dysfunction and sarcopenia of aging are linked to altered organelle dynamics, providing a context in which peroxisome fission may contribute to age-related decline. Mitochondrial energetics in the kidney depend on balanced fission and fusion, and shared machinery suggests peroxisome fission is relevant there as well. In neurodegeneration, pathways such as AMPK/PGC-1alpha/SIRT3 regulate mitophagy and organelle quality control, overlapping with the regulation of fission. Together these areas define the disease landscape for GO:0016559.
From peroxisome fission-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is MFF required for peroxisome fission? | MFF knockout cell line |
| Does a patient variant impair fission? | Point-mutation knock-in cell line |
| Where does MFF localize during fission? | Tagged knock-in with fluorescent tag |
| Does increased fission factor drive peroxisome proliferation? | Overexpression cell model |
| Does fission loss alter lipid metabolism? | Knockout plus lipidomics |
| Does fission loss change mitochondrial dynamics? | Knockout with mitochondrial imaging |
How to Study the peroxisome fission Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Fluorescence microscopy | Peroxisome number and division events | Quantifying GO:0016559 activity |
| Live-cell imaging | Membrane constriction and separation | Visualizing fission dynamics |
| CRISPR knockout | Requirement of a gene for fission | Testing MFF dependence |
| Knock-in tagging | Localization of fission factors | Tracking MFF at peroxisomes |
| Lipidomics | Peroxisome-derived lipid species | Linking fission to thermogenesis |
| Metabolic flux assays | Fatty acid metabolism | Cancer metabolic reprogramming |
| Mitophagy assays | Organelle quality control | Stress pathway readouts |
| Mitochondrial dynamics imaging | Fission and fusion balance | Shared machinery studies |
Imaging peroxisome dynamics
Fluorescence imaging of peroxisome markers is used to quantify peroxisome number, size, and division events, which are the direct readouts of GO:0016559. Tagged knock-in of fission factors such as MFF allows their localization to be tracked during division. Live-cell imaging can capture constriction and separation of peroxisomal compartments.
Genetic perturbation with CRISPR
CRISPR knockout of fission genes such as MFF is used to test whether a factor is required for peroxisome division. Point-mutation knock-in can model disease-associated variants that alter fission activity. Overexpression models test whether increased fission factor abundance drives peroxisome proliferation.
Metabolic and lipid profiling
Because peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission, lipidomics and metabolic assays are used to connect fission to metabolism. Fatty acid metabolism reprogramming in cancer cells can be measured to link fission to tumor metabolism. These approaches place GO:0016559 within a metabolic network.
Organelle dynamics and stress assays
Mitochondrial dynamics assays are used alongside peroxisome assays because the two systems share components such as MFF. Mitophagy and stress-response pathways involving AMPK, PGC-1alpha, and SIRT3 provide readouts for organelle quality control. Kidney and muscle models provide physiological contexts for organelle dynamics studies.
How CRISPR Can Be Used to Study GO:0016559 peroxisome fission
Knockout
CRISPR knockout of MFF and related genes is used to test whether a factor is required for peroxisome fission, since MFF is a critical regulator of peroxisome maturation and division. Knockout models of peroxisome dynamics genes help define the minimal machinery for GO:0016559. These models are also used to assess secondary effects on mitochondrial dynamics.
Point Mutation
Point-mutation knock-in models are used to test whether specific residues in fission factors are required for peroxisome division. Such models help distinguish loss-of-function from separation-of-function effects in organelle dynamics. They are particularly useful for modeling disease-associated variants in peroxisome dynamics genes.
Knock-in
Tagged knock-in of fission factors such as MFF allows localization and interaction studies at endogenous expression levels. Knock-in reporters can be used to monitor peroxisome division in real time. These models support precise dissection of GO:0016559 in physiologically relevant contexts.
Overexpression
Overexpression of fission factors is used to test whether increased activity drives peroxisome proliferation and division. Overexpression models can reveal dominant effects of fission proteins on organelle number and size. They complement knockout studies by testing sufficiency rather than requirement.
How EDITGENE Supports peroxisome fission Research
Researchers studying peroxisome fission-related genes often need to determine whether a candidate gene is causally involved in peroxisome division, whether a specific variant alters fission activity, and how the gene behaves when tagged or overexpressed. EDITGENE provides the CRISPR cell models and screening services needed to answer these questions with publication-grade rigor.
Contact EDITGENE today to design your custom CRISPR model for peroxisome fission research.
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ACOX1 Knockout HEK293 Cell Line | EDJ-KQ1810 | Human | 51 | Details Get a Quote |
| PEX19 Knockout HEK293 Cell Line | EDJ-KQ5611 | Human | 5824 | Details Get a Quote |
| PEX11B Knockout HEK293 Cell Line | EDJ-KQ6365 | Human | 8799 | Details Get a Quote |
| PEX11A Knockout HEK293 Cell Line | EDJ-KQ6366 | Human | 8800 | Details Get a Quote |
| ACOT8 Knockout HEK293 Cell Line | EDJ-KQ6860 | Human | 10005 | Details Get a Quote |
| SEC16B Knockout HEK293 Cell Line | EDJ-KQ10527 | Human | 89866 | Details Get a Quote |
| FIS1 Knockout HEK293 Cell Line | EDJ-KQ10875 | Human | 51024 | Details Get a Quote |
| PEX11G Knockout HEK293 Cell Line | EDJ-KQ11123 | Human | 92960 | Details Get a Quote |
| MFF Knockout HEK293 Cell Line | EDJ-KQ11968 | Human | 56947 | Details Get a Quote |
| PEX11B Knockout A-549 Cell Line | EDJ-KQ29021 | Human | 8799 | Details Get a Quote |
| SEC16B Knockout A-549 Cell Line | EDJ-KQ37948 | Human | 89866 | Details Get a Quote |
| PEX11G Knockout A-549 Cell Line | EDJ-KQ39104 | Human | 92960 | Details Get a Quote |
| ACOX1 Knockout HCT 116 Cell Line | EDJ-KQ20340 | Human | 51 | Details Get a Quote |
| ACOX1 Knockout A-549 Cell Line | EDJ-KQ21661 | Human | 51 | Details Get a Quote |
| ACOX1 Knockout HeLa Cell Line | EDJ-KQ21662 | Human | 51 | Details Get a Quote |
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Frequently Asked Questions About peroxisome fission
What is peroxisome fission?
Peroxisome fission (GO:0016559) is the division of a mature peroxisome within a cell to form two or more separate peroxisome compartments.
What genes are involved in peroxisome fission?
Key genes include MFF, a critical regulator of peroxisome maturation and division, along with dynamin-related fission machinery and peroxisomal membrane proteins.
Why is peroxisome fission important?
It maintains peroxisome number and function, and its failure contributes to disorders of peroxisome dynamics and metabolic disease.
How is peroxisome fission related to mitochondrial fission?
The two processes share components such as MFF, and peroxisome-derived lipids regulate cold-induced mitochondrial fission in adipose tissue.
What diseases are linked to peroxisome fission defects?
Disorders of peroxisome dynamics are linked to neurological and metabolic disease, and fission dynamics are also relevant to cancer metabolism.
What is the GO ID for peroxisome fission?
The GO ID is GO:0016559, a biological process term.
What are synonyms for peroxisome fission?
The synonyms are peroxisome division and peroxisome proliferation.
How do researchers study peroxisome fission?
They use fluorescence imaging, CRISPR knockout, knock-in tagging, lipidomics, and metabolic assays.
Can peroxisome fission be studied with CRISPR?
Yes, CRISPR knockout, point-mutation, knock-in, and overexpression models are used to test the role of fission genes such as MFF.
Is peroxisome fission the same as peroxisome biogenesis?
No, peroxisome fission specifically refers to division of a mature peroxisome, whereas biogenesis includes formation and growth of peroxisomes.
Conclusion
GO:0016559 peroxisome fission is the biological process that divides mature peroxisomes into separate compartments, and it is essential for peroxisome propagation and cellular metabolism. Its machinery, including the critical regulator MFF, is shared with mitochondrial dynamics, and its activity is coupled to thermogenesis and metabolic reprogramming. Defects in peroxisome fission contribute to disorders of peroxisome dynamics and are relevant to cancer, kidney, and aging biology. CRISPR-based knockout, point-mutation, knock-in, and overexpression models provide the experimental toolkit needed to dissect this process and its disease connections.
References
- 1. Park H et al.. 2019. Peroxisome-derived lipids regulate adipose thermogenesis by mediating cold-induced mitochondrial fission.. J Clin Invest 129(2):694-711 PMID: 30511960
- 2. Carmichael RE et al.. 2022. Fission Impossible (?)-New Insights into Disorders of Peroxisome Dynamics.. Cells 11(12) PMID: 35741050
- 3. Bhargava P et al.. 2017. Mitochondrial energetics in the kidney.. Nat Rev Nephrol 13(10):629-646 PMID: 28804120
- 4. Wang Y et al.. 2025. Aloe-Emodin Improves Mitophagy in Alzheimer's Disease via Activating the AMPK/PGC-1α/SIRT3 Signaling Pathway.. CNS Neurosci Ther 31(3):e70346 PMID: 40125832
- 5. Wu D et al.. 2022. Increased mitochondrial fission drives the reprogramming of fatty acid metabolism in hepatocellular carcinoma cells through suppression of Sirtuin 1.. Cancer Commun (Lond) 42(1):37-55 PMID: 34981667
- 6. Halling JF et al.. 2020. PGC-1α-mediated regulation of mitochondrial function and physiological implications.. Appl Physiol Nutr Metab 45(9):927-936 PMID: 32516539
- 7. Marzetti E et al.. 2013. Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials.. Int J Biochem Cell Biol 45(10):2288-301 PMID: 23845738
- 8. Passmore JB et al.. 2020. Mitochondrial fission factor (MFF) is a critical regulator of peroxisome maturation.. Biochim Biophys Acta Mol Cell Res 1867(7):118709 PMID: 32224193
