GO:0062037 D-loop DNA binding: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0062037 (D-loop DNA binding) describes the molecular function of binding a three-stranded DNA displacement loop (D-loop), a structure in which an invading single strand base-pairs with one strand of duplex DNA while the rest of the duplex remains unwound.
• D-loops are central intermediates of homologous recombination and homology-directed repair, and are also the defining structural feature of the mitochondrial displacement loop and of telomeric D-loop/T-loop architecture.
• RecA-family recombinases (RecA in bacteria, RAD51 in eukaryotes) catalyze the strand-invasion reaction that creates D-loops, and structural studies have resolved RecA-DNA and RAD51-DNA synaptic and D-loop conformations.
• D-loop DNA binding proteins include mitochondrial D-loop-binding factors such as mitochondrial histones and HMGA2, which bind the mitochondrial D-loop region and influence mitochondrial gene expression and metabolism.
• D-loop region variation and methylation are used as markers in mitochondrial disease and neurodegeneration research, including amyotrophic lateral sclerosis (ALS) mutation carriers.
• D-loop DNA binding can be interrogated with biochemical binding assays, single-molecule and structural methods, mitochondrial D-loop proteomics, and CRISPR-engineered cell models.
Description
D-loop DNA binding (GO:0062037) is the molecular function of binding to a DNA D-loop, a three-stranded DNA structure formed when a single DNA strand invades duplex DNA and base-pairs with one of the two strands while the remainder of the duplex does not unwind. This non-canonical DNA architecture is not a rare curiosity: it is the physical intermediate through which homologous recombination and homology-directed DNA repair proceed, and it is also the structural signature of the mitochondrial displacement loop and of telomeric D-loop/T-loop organization. Because D-loops sit at the intersection of DNA repair, replication, and genome stability, the proteins that create, stabilize, or bind them are of broad interest to researchers in cancer biology, mitochondrial genetics, and aging. The term is defined in QuickGO as binding to a DNA D-loop, with the synonym DNA displacement loop binding, and it is classified under the molecular_function aspect of the Gene Ontology. In practice, D-loop DNA binding is studied both as a biochemical activity of purified recombinases and as a property of mitochondrial and nuclear proteins that associate with D-loop-containing DNA in cells. Understanding this function therefore requires combining structural biology, single-molecule biochemistry, and cell-based perturbation of the genes encoding D-loop-binding proteins.
D-loop DNA binding At A Glance
| GO ID | GO:0062037 |
|---|---|
| GO term | D-loop DNA binding |
| Ontology | molecular_function |
| Synonym | DNA displacement loop binding |
| Definition | Binding to a DNA D-loop, a three-stranded DNA structure formed by invasion of a single DNA strand that base pairs with one strand of duplex DNA while the rest of the double-stranded DNA does not unwind |
| Major function | Recognition and binding of three-stranded D-loop DNA intermediates generated during strand invasion, homologous recombination, and mitochondrial D-loop formation |
| Representative binders | RecA-family recombinases (RecA, RAD51), mitochondrial D-loop-binding proteins including mitochondrial histones and HMGA2 |
| Associated processes | Homologous recombination, homology-directed repair, mitochondrial DNA replication and transcription, telomeric D-loop/T-loop biology |
| Research relevance | Cancer genome stability, mitochondrial disease and neurodegeneration markers, and mechanistic studies of strand exchange |
What Is GO:0062037?
In plain terms, D-loop DNA binding (GO:0062037) means a protein physically associates with a DNA D-loop, the three-stranded structure created when one DNA strand invades a DNA duplex and pairs with one of its strands while the other strand is displaced but the duplex itself does not unwind. The QuickGO definition specifies binding to this D-loop DNA structure, and the accepted synonym is DNA displacement loop binding. Functionally, this activity is distinct from generic single-stranded or double-stranded DNA binding because the ligand is a specific three-stranded conformation whose geometry and base-pairing register determine which proteins can recognize it. D-loop DNA binding underlies processes such as RecA/RAD51-mediated strand exchange, mitochondrial D-loop maintenance, and telomeric D-loop/T-loop function.
Why Is D-loop DNA binding Important in Cell Biology?
D-loop DNA binding matters because the D-loop is the point at which a DNA strand is physically exchanged between duplexes, making it the decisive intermediate of homologous recombination and homology-directed repair. Proteins that bind D-loops therefore govern how cells repair breaks, restart stalled replication, and maintain genome stability, and their dysfunction is linked to cancer predisposition and to mitochondrial and neurodegenerative phenotypes. In mitochondria, the displacement loop is a defining feature of the control region, and proteins that bind this region, including mitochondrial histones and HMGA2, influence mitochondrial gene expression and metabolic state. In telomere biology, D-loop/T-loop structures are central to how chromosome ends are protected and regulated. For researchers, GO:0062037 provides a precise annotation target for assigning function to recombinases, mitochondrial DNA-binding proteins, and any factor that recognizes three-stranded DNA, and it connects structural mechanism to disease-relevant phenotypes.
• D-loops are the essential intermediate of RecA/RAD51-catalyzed strand exchange, so D-loop DNA binding is directly tied to homologous recombination and homology-directed repair.
• Structural resolution of RecA-DNA synaptic and D-loop states and of eukaryotic RAD51 D-loop structures has made D-loop binding a mechanistically tractable function to study.
• The mitochondrial displacement loop is a hotspot for variation and methylation, and D-loop region changes are studied in ALS mutation carriers and other mitochondrial phenotypes.
• HMGA2 binds the mitochondrial D-loop region and mediates Cr(VI)-induced metabolic reprogramming, linking D-loop binding to environmental stress responses.
• Proteomic identification of mitochondrial D-loop DNA-binding proteins, including mitochondrial histones, shows that D-loop binding is a defined biochemical activity amenable to discovery workflows.
• D-loop/R-loop-dependent replication mechanisms in Escherichia coli connect D-loop binding to primer RNA synthesis and replication initiation.
• Telomeric D-loop/T-loop architecture places D-loop binding in the context of chromosome-end protection and telomere regulation.
• Because D-loop binding proteins influence repair fidelity, they are candidate targets and biomarkers in cancer and genome-stability research.
• D-loop DNA binding can be perturbed genetically with CRISPR knockout, point mutation, knock-in, and overexpression models to test causality.
• The function is assayable by biochemical binding, structural, single-molecule, and proteomic methods, making it suitable for multi-modal research programs.
What Happens During D-loop DNA binding?
Strand invasion and D-loop formation
In simple terms: One DNA strand invades a double helix and pairs with one of its strands, pushing the other strand aside to create a three-stranded loop.
D-loop DNA binding begins with the formation of the D-loop itself. A single DNA strand invades duplex DNA and base-pairs with one strand of the duplex, while the rest of the double-stranded DNA does not unwind, producing the three-stranded D-loop structure that defines the ligand for GO:0062037. In bacteria, RecA catalyzes this strand-exchange reaction, and structural studies of RecA-DNA synaptic and D-loop complexes have revealed how the invading strand is positioned within the recombinase filament. In eukaryotes, RAD51 performs the analogous reaction, and RAD51 D-loop structures have been resolved to show the mechanism of eukaryotic RAD51-mediated strand exchange. D-loop/R-loop-dependent replication mechanisms in Escherichia coli further illustrate how these structures can serve as substrates for primer RNA synthesis and replication initiation.
Recognition and stable binding of the D-loop
In simple terms: Proteins that can read the three-stranded shape grab onto the D-loop and hold it.
Once formed, the D-loop is recognized by proteins whose binding specificity is directed at the three-stranded conformation rather than at generic single- or double-stranded DNA. RecA-family recombinases remain bound to the product of strand exchange, and the resolved synaptic and D-loop structures show the protein-DNA contacts that stabilize the invaded strand. In mitochondria, D-loop DNA-binding proteins have been identified by shot-gun proteomics of mitochondrial D-loop DNA, revealing factors such as mitochondrial histones that associate with this region. HMGA2 also binds the mitochondrial D-loop region, demonstrating that non-recombinase proteins can use D-loop binding as part of a regulatory program.
D-loop binding in mitochondrial DNA biology
In simple terms: In mitochondria, the displacement loop is a normal feature of the control region, and proteins that bind it help regulate mitochondrial DNA.
The mitochondrial displacement loop is a stable three-stranded region in the mitochondrial control region, and D-loop DNA binding is therefore part of normal mitochondrial DNA biology. Mitochondrial D-loop DNA-binding proteins identified by proteomics include mitochondrial histones, indicating that D-loop binding contributes to the organization of mitochondrial DNA. HMGA2 binding to the mitochondrial D-loop region has been linked to Cr(VI)-induced metabolic reprogramming, connecting D-loop occupancy to metabolic gene expression. Variation and methylation of the mitochondrial D-loop region are used as readouts in disease research, including studies of ALS gene mutation carriers.
D-loop binding at telomeres
In simple terms: At chromosome ends, D-loop-like structures help protect and regulate telomeres.
Telomeres form D-loop/T-loop structures, and the concept that telomeres do D-loop-T-loop work places D-loop binding within the framework of chromosome-end protection and telomere regulation. This extends the relevance of GO:0062037 beyond recombination and mitochondria to the specialized nucleoprotein architecture of telomeres. Because telomeric D-loop/T-loop organization is tied to telomere maintenance, proteins that bind these structures are of interest in aging and cancer research.
Key Genes Involved in GO:0062037 D-loop DNA binding
The genes and proteins most directly associated with D-loop DNA binding include RecA-family recombinases, mitochondrial D-loop-binding factors, and telomere-associated proteins, as supported by the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| recA | Bacterial recombinase that catalyzes strand invasion and forms RecA-DNA synaptic and D-loop structures | Structural and mechanistic studies of D-loop formation and D-loop DNA binding |
| RAD51 | Eukaryotic recombinase that mediates strand exchange and forms RAD51 D-loop structures | Mechanistic studies of eukaryotic RAD51-mediated strand exchange and D-loop binding |
| HMGA2 | Binds the mitochondrial D-loop region and mediates Cr(VI)-induced metabolic reprogramming | Links D-loop binding to environmental stress and metabolic reprogramming |
| Mitochondrial histones | Mitochondrial D-loop DNA-binding proteins identified by shot-gun proteomics | Discovery of D-loop-binding factors in mitochondria |
| TIN2 | Telomere-associated protein implicated in mitochondrial shuttling and oxidative stress responses | Connects telomere/mitochondrial biology to stress-induced apoptosis |
| FOXO1 | Transcription factor whose mitochondrial shuttling is modulated by TIN2 | Context for mitochondrial stress and apoptosis studies relevant to D-loop biology |
| Mitochondrial D-loop region (control region) | Contains the displacement loop and is a hotspot for variation and methylation | Disease marker studies including ALS mutation carriers |
| D-loop/R-loop-dependent replication machinery (E. coli) | Supports primer RNA synthesis and replication initiation | Mechanistic studies of D-loop/R-loop-dependent replication |
| Telomeric D-loop/T-loop components | Form and regulate telomeric D-loop/T-loop structures | Telomere protection and regulation research |
| RecA-family recombinase accessory factors | Support recombinase filament function and strand exchange | Biochemical dissection of D-loop DNA binding |
| Mitochondrial DNA-binding proteins (proteomic set) | Bind mitochondrial D-loop DNA | Proteomic identification of D-loop-binding proteins |
| Cr(VI)-response pathway components | Mediate metabolic reprogramming downstream of HMGA2 D-loop binding | Toxicology and metabolic reprogramming studies |
| ALS-associated gene products | Studied in carriers with mitochondrial D-loop copy number and methylation changes | Neurodegeneration biomarker research |
| Telomere maintenance factors | Maintain telomeric D-loop/T-loop architecture | Aging and cancer research |
| Homologous recombination repair factors | Function in homology-directed repair involving D-loop intermediates | Genome stability and cancer research |
| Mitochondrial stress-response factors | Respond to oxidative stress in mitochondria | Retinal pigment epithelium and hyperglycemia models |
How Is D-loop DNA binding Regulated?
D-loop DNA binding is regulated at the level of D-loop formation and stability, which depends on the activity of RecA-family recombinases and on the proteins that associate with the resulting three-stranded structure. In mitochondria, D-loop occupancy by factors such as HMGA2 and mitochondrial histones is influenced by cellular and environmental conditions, including exposure to Cr(VI) and metabolic state. Telomeric D-loop/T-loop architecture is likewise subject to regulation as part of telomere maintenance. Mitochondrial stress pathways involving TIN2 and FOXO1 provide additional context in which mitochondrial DNA-associated functions are modulated under oxidative stress.
D-loop DNA binding and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| RAD51 | Homologous recombination and genome stability in cancer | RAD51 knockout and point-mutation cell lines with D-loop binding assays |
| recA | Bacterial recombination and replication mechanisms | Recombinase point mutants and in vitro D-loop formation assays |
| HMGA2 | Cr(VI)-induced metabolic reprogramming and mitochondrial D-loop binding | HMGA2 overexpression and knockout cells with mitochondrial D-loop readouts |
| Mitochondrial D-loop region | ALS and mitochondrial disease marker studies | Patient-derived cells and mitochondrial D-loop copy number/methylation assays |
| TIN2 / FOXO1 | Oxidative stress-induced apoptosis in retinal pigment epithelium under hyperglycemia | TIN2 or FOXO1 perturbation in retinal pigment epithelium models |
Cancer and genome instability
Because D-loops are intermediates of homologous recombination and homology-directed repair, proteins that bind D-loop DNA are mechanistically linked to the fidelity of DNA repair and to genome stability. Defects in these pathways are a general theme in cancer biology, and the structural and biochemical characterization of RecA-DNA and RAD51-DNA D-loop complexes provides a foundation for interpreting how repair defects arise. D-loop DNA binding is therefore a relevant annotation for genes whose perturbation alters repair outcomes in cancer models.
Mitochondrial disease and neurodegeneration
The mitochondrial displacement loop is a hotspot for variation and methylation, and D-loop region copy number and methylation have been examined in carriers of amyotrophic lateral sclerosis gene mutations. Proteins that bind the mitochondrial D-loop region, including HMGA2 and mitochondrial histones, influence mitochondrial gene expression and metabolic state, providing a mechanistic route from D-loop binding to mitochondrial phenotypes. These observations support the use of mitochondrial D-loop readouts in neurodegeneration and mitochondrial disease research.
Metabolic and oxidative stress-related disease
HMGA2 binding to the mitochondrial D-loop region mediates Cr(VI)-induced metabolic reprogramming, linking D-loop DNA binding to metabolic responses under environmental stress. In parallel, TIN2 modulates FOXO1 mitochondrial shuttling to enhance oxidative stress-induced apoptosis in retinal pigment epithelium under hyperglycemia, illustrating how mitochondrial stress pathways intersect with DNA-associated functions. Together these findings connect D-loop biology to metabolic and oxidative stress-related disease contexts.
Telomere-related aging and disease
Telomeres form D-loop/T-loop structures, and the concept that telomeres do D-loop-T-loop work ties D-loop biology to chromosome-end protection and telomere regulation. Because telomere dysfunction is associated with aging and cancer, proteins that bind telomeric D-loop/T-loop structures are of interest in these disease areas. This extends the disease relevance of GO:0062037 beyond recombination and mitochondria.
From D-loop DNA binding-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for D-loop DNA binding? | CRISPR knockout cell line with biochemical D-loop binding assay |
| Does a specific residue mediate D-loop recognition? | Point-mutation knock-in of the candidate residue followed by binding assays |
| Does tagging alter D-loop binding localization? | Tagged knock-in of the endogenous locus for imaging and pulldown |
| Does increased dosage of a D-loop-binding factor change phenotype? | Overexpression cell model with mitochondrial or nuclear D-loop readouts |
| Which proteins bind the mitochondrial D-loop? | Mitochondrial D-loop DNA proteomics in wild-type and perturbed cells |
| Does D-loop region variation affect disease-relevant readouts? | Patient-derived cells with mitochondrial D-loop copy number and methylation assays |
How to Study the D-loop DNA binding Process
| Method | What It Measures | Typical Application |
|---|---|---|
| D-loop formation/strand-exchange assay | Ability of a protein to create and bind D-loop DNA | Functional testing of recombinases and mutants |
| Structural biology (cryo-EM/crystallography) | Three-dimensional architecture of protein-DNA D-loop complexes | Residue-level mechanism of D-loop recognition |
| Mitochondrial D-loop DNA proteomics | Proteins that bind the mitochondrial D-loop | Discovery of D-loop-binding factors such as mitochondrial histones |
| Mitochondrial DNA copy number assay | Amount of mitochondrial DNA | Disease marker studies in ALS mutation carriers |
| D-loop region methylation assay | Methylation status of the mitochondrial D-loop | Epigenetic studies in neurodegeneration |
| Binding assays with HMGA2 | Association of HMGA2 with the mitochondrial D-loop region | Metabolic reprogramming and stress-response studies |
| Oxidative stress and apoptosis assays | Stress-induced apoptosis in relevant cell types | TIN2/FOXO1 mitochondrial shuttling studies |
| Telomere D-loop/T-loop analysis | Telomeric D-loop/T-loop architecture | Telomere protection and regulation research |
Biochemical D-loop binding and strand-exchange assays
D-loop DNA binding can be measured directly using strand-exchange and D-loop formation assays with purified recombinases, as demonstrated by structural and biochemical studies of RecA-DNA synaptic and D-loop complexes and of RAD51 D-loop structures. These assays define whether a protein or mutant retains the ability to bind the three-stranded product of strand invasion. They are the primary functional readout for GO:0062037 in vitro.
Structural biology of D-loop complexes
Structural determination of RecA-DNA synaptic and D-loop structures and of eukaryotic RAD51 D-loop structures provides residue-level insight into how D-loop DNA is recognized. Such structures reveal the geometry of the three-stranded ligand and the protein contacts that stabilize it. They are essential for interpreting the functional consequences of point mutations in D-loop-binding proteins.
Mitochondrial D-loop proteomics
Shot-gun proteomic analysis of mitochondrial D-loop DNA binding proteins has been used to identify factors that associate with the mitochondrial D-loop, including mitochondrial histones. This approach enables unbiased discovery of D-loop-binding proteins in mitochondria. It complements candidate-based biochemical assays and can be combined with genetic perturbation.
Mitochondrial D-loop copy number and methylation assays
Mitochondrial DNA copy number and D-loop region methylation are measurable readouts used in studies of ALS gene mutation carriers. These assays connect D-loop biology to disease-relevant mitochondrial phenotypes. They are useful when evaluating whether a D-loop-binding factor influences mitochondrial DNA regulation.
How CRISPR Can Be Used to Study GO:0062037 D-loop DNA binding
Knockout
CRISPR knockout of genes encoding candidate D-loop-binding proteins allows researchers to test whether the protein is required for D-loop DNA binding and for downstream processes such as homologous recombination or mitochondrial DNA regulation. Knockout cell lines can be interrogated with biochemical D-loop binding assays and mitochondrial D-loop proteomics to determine loss of function. This is the most direct way to establish causality for a gene annotated with GO:0062037.
Point Mutation
Point-mutation models are used to dissect which residues mediate D-loop recognition, guided by structural data on RecA-DNA and RAD51-DNA D-loop complexes. Introducing specific missense changes into the endogenous locus allows separation of D-loop binding from other activities of the protein. Such models are valuable when a domain is multifunctional and a clean separation of function is needed.
Knock-in
Knock-in of tags or reporter sequences at the endogenous locus enables visualization and affinity capture of D-loop-binding proteins in their native context. Tagged knock-in lines can be used for imaging of mitochondrial or nuclear D-loop association and for pulldown-based interaction studies. This complements proteomic identification of mitochondrial D-loop-binding proteins.
Overexpression
Overexpression models test whether increased dosage of a D-loop-binding factor alters D-loop-dependent phenotypes, such as mitochondrial gene expression or metabolic reprogramming. For example, HMGA2 binding to the mitochondrial D-loop region is linked to Cr(VI)-induced metabolic reprogramming, making overexpression a suitable perturbation for this axis. Overexpression can also be combined with stress treatments to reveal context-dependent effects.
How EDITGENE Supports D-loop DNA binding Research
Researchers studying D-loop DNA binding-related genes often need to determine whether a candidate gene is causally involved in D-loop recognition, D-loop-dependent repair, or mitochondrial D-loop regulation, and CRISPR-engineered cell models provide a rigorous way to test that causality.
Contact EDITGENE today to design your custom CRISPR model for D-loop DNA binding research.
Frequently Asked Questions About D-loop DNA binding
What is D-loop DNA binding?
D-loop DNA binding (GO:0062037) is the molecular function of binding to a DNA D-loop, a three-stranded DNA structure formed when an invading single strand base-pairs with one strand of duplex DNA while the rest of the duplex does not unwind.
What is the GO ID for D-loop DNA binding?
The Gene Ontology ID for D-loop DNA binding is GO:0062037, classified under the molecular_function aspect, with the synonym DNA displacement loop binding.
What genes are involved in D-loop DNA binding?
Key genes and proteins include RecA-family recombinases such as recA and RAD51, the mitochondrial D-loop-binding factor HMGA2, and mitochondrial D-loop DNA-binding proteins such as mitochondrial histones.
How is a D-loop formed?
A D-loop forms when a single DNA strand invades duplex DNA and base-pairs with one strand while the rest of the double-stranded DNA does not unwind, a reaction catalyzed by RecA-family recombinases.
Why is D-loop DNA binding important for homologous recombination?
D-loops are the essential intermediate of RecA/RAD51-catalyzed strand exchange, so proteins that bind D-loop DNA directly govern homologous recombination and homology-directed repair.
What is the mitochondrial D-loop?
The mitochondrial displacement loop is a three-stranded region in the mitochondrial control region that is bound by proteins such as HMGA2 and mitochondrial histones and is studied as a marker in mitochondrial disease and neurodegeneration.
Is D-loop DNA binding relevant to ALS?
Mitochondrial DNA copy number and D-loop region methylation have been examined in carriers of amyotrophic lateral sclerosis gene mutations, linking D-loop biology to neurodegeneration research.
How do you measure D-loop DNA binding?
Common approaches include biochemical D-loop formation and strand-exchange assays, structural biology of protein-DNA D-loop complexes, and mitochondrial D-loop proteomics.
How do telomeres relate to D-loops?
Telomeres form D-loop/T-loop structures, and the concept that telomeres do D-loop-T-loop work connects D-loop biology to chromosome-end protection and telomere regulation.
How can CRISPR help study D-loop DNA binding?
CRISPR knockout, point mutation, knock-in, and overexpression models allow researchers to test whether specific genes and residues are required for D-loop DNA binding and its downstream functions.
Conclusion
D-loop DNA binding (GO:0062037) is a precise molecular function annotation for proteins that recognize the three-stranded D-loop intermediate of strand invasion. Its importance spans homologous recombination and genome stability, mitochondrial D-loop biology, and telomeric D-loop/T-loop architecture, with disease relevance in cancer, neurodegeneration, and metabolic stress contexts. Combining structural, biochemical, proteomic, and CRISPR-based approaches provides a rigorous path to assign and test this function in candidate genes.
References
- 1. Greider CW. 1999. Telomeres do D-loop-T-loop.. Cell 97(4):419-22 PMID: 10338204
- 2. Yang H et al.. 2020. Mechanism of strand exchange from RecA-DNA synaptic and D-loop structures.. Nature 586(7831):801-806 PMID: 33057191
- 3. Luo SC et al.. 2025. RAD51 D-loop structures reveal the mechanism of eukaryotic RAD51-mediated strand exchange.. Nat Commun 17(1):243 PMID: 41326376
- 4. Stoccoro A et al.. 2018. Mitochondrial DNA copy number and D-loop region methylation in carriers of amyotrophic lateral sclerosis gene mutations.. Epigenomics 10(11):1431-1443 PMID: 30088417
- 5. Bao S et al.. 2022. HMGA2 mediates Cr (VI)-induced metabolic reprogramming through binding to mitochondrial D-Loop region.. Ecotoxicol Environ Saf 244:114085 PMID: 36116352
- 6. Masai H et al.. 1996. Mechanisms of primer RNA synthesis and D-loop/R-loop-dependent DNA replication in Escherichia coli.. Biochimie 78(11-12):1109-17 PMID: 9150892
- 7. Chen S et al.. 2024. TIN2 modulates FOXO1 mitochondrial shuttling to enhance oxidative stress-induced apoptosis in retinal pigment epithelium under hyperglycemia.. Cell Death Differ 31(11):1487-1505 PMID: 39080375
- 8. Choi YS et al.. 2011. Shot-gun proteomic analysis of mitochondrial D-loop DNA binding proteins: identification of mitochondrial histones.. Mol Biosyst 7(5):1523-36 PMID: 21359316
