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Scan for outdated or missing drivers - takes under a minuteDriver Scan →Clear out junk files and repair common Windows errorsFree Scan →Fix the driver behind crashes, sound loss and screen glitchesFind Drivers →Human mitochondrial DNA (mtDNA) is usually inherited from the mother, but it is not passed down as an identical, unchanging set of copies. When a person carries more than one mtDNA variant—a state called heteroplasmy—random sampling and segregation can alter the variants’ proportions across cells, tissues and generations. Selection can also shift those proportions, but its effects depend on the variant and biological setting.
How is mitochondrial DNA inherited?
Human mtDNA is generally transmitted through the maternal line. Reports that seem to show inheritance from both parents require careful interpretation: a paternal allele may have entered through the nuclear genome rather than through paternal mtDNA. A review of human inheritance and disease discusses this distinction and its implications (Chinnery and colleagues, 2021).
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According to a 2026 review in the Annual Review of Genomics and Human Genetics, human mtDNA is a circular molecule 16,569 base pairs long and encodes 13 proteins essential to oxidative phosphorylation (Ryall, Chinnery and van den Ameele, 2026). Cells contain many mtDNA copies, and those copies need not all have the same sequence.
What is heteroplasmy?
Heteroplasmy means that a cell or person has a mixture of mtDNA variants—for example, copies with a particular mutation alongside copies without it. The proportion of copies carrying a variant is its heteroplasmy level. That proportion can differ between cells and tissues in one person, and it can change as cells divide or across generations.
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Consequently, a measurement from one tissue does not necessarily describe every other tissue or predict the variant level in a future generation. Differences among offspring can arise even when they have the same mother, because each inherits a different sample of her mtDNA population and subsequent changes can further alter variant proportions.
What is the mitochondrial genetic bottleneck?
During oogenesis, the number of mtDNA copies contributing to the developing germline can fall sharply. This bottleneck narrows the pool that is sampled and can increase the chance that different eggs receive substantially different proportions of mtDNA variants. The bottleneck does not mean every egg receives the same fixed number of copies; the reviewed evidence does not establish one universal bottleneck size.
After the sample is established, mtDNA copies replicate and are partitioned as cells develop. This segregation can preserve or amplify differences that began in the bottleneck, producing variation among eggs and, ultimately, among siblings. A 2026 review describes bottlenecks as intensifying stochastic variation in both germline and somatic settings (Xie, Walker, Minczuk and colleagues, 2026).
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Two processes need to be distinguished:
- Stochastic drift changes variant proportions through chance sampling, replication and segregation. It is not inherently a shift toward healthier or more harmful mtDNA.
- Selection produces a directional shift associated with the effects of a variant, mitochondrion or cell. Its direction and strength depend on the biological context.
Relaxed replication and vegetative segregation—the sorting of mtDNA variants among dividing cells—can contribute to random changes. A narrow germline sampling pool can magnify their effects. Selection may then act alongside drift, so sibling differences cannot be attributed to a single process in every case.
How does selection change mitochondrial DNA heteroplasmy?
Purifying selection describes processes that reduce deleterious mtDNA variants or lessen their functional consequences. It is not a guarantee that every harmful variant will be removed. A 2026 synthesis identifies mitochondrial quality control as an important setting for within-cell purifying selection and discusses mechanisms including mitophagy and preferential replication (Xie, Walker, Minczuk and colleagues, 2026).
Within-cell quality control
Mitophagy is the selective removal of mitochondria. If quality-control processes preferentially remove mitochondria associated with a deleterious variant, the variant’s representation may fall within a cell. Preferential replication could also change the relative abundance of mtDNA variants. These mechanisms are areas of study, not one settled pathway that applies uniformly to every mutation, cell type or organism.
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Differences among cells
Selection can also operate through differences among cells: cells whose mitochondrial populations function differently may fare differently as tissues develop or renew. This intercellular competition is distinct from quality control within a cell. Germline and somatic tissues also present different settings for these processes; a mechanism or effect observed in one does not automatically explain inheritance or variant dynamics in another.
The 2026 review summarizes the relationship this way: “Stochastic processes (relaxed replication and vegetative segregation, enhanced through genetic bottlenecks) generate cell-to-cell variation, while selection mechanisms such as intercellular competition, mitophagy, and preferential replication allow or drive directional shifts.” (Ryall, Chinnery and van den Ameele, 2026.)
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What does this mean for mitochondrial disease?
Disease risk and severity depend on the particular variant and context, including where in the body it is present and how its level changes. Heteroplasmy helps explain why people carrying the same mtDNA variant can have different clinical outcomes, including differences among offspring. A single percentage is not a universal threshold for predicting whether someone will develop disease or how severe it will be; the cited reviews do not establish one cutoff that applies across variants and tissues.
Inheritance patterns therefore reflect both sampling and biological change: maternal transmission is the general rule, while bottlenecks and segregation create variation and selection can shift it. Neither random drift nor any single proposed selection mechanism accounts for every observed pattern.
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