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Comment by JohnJamesRambo | Hacker News Reader

How do you know paternal mitochondrial dna transmission isn’t so rare that it has no real measurable effect on population mapping?

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In humans between 1 in 1000 and 1 in 10,000 of the mtDNA is copied from the father, and how much and which parts seems to depend a lot on the particular father, perhaps suggesting that there exists an as yet undiscovered checksum scheme, and not random chance. Most mtDNA between humans is the same, and mtDNA is only 16,569 base pairs long. So in most offspring the paternal mtDNA contribution of 1-20 base pairs happens to be the same as the maternal mtDNA and one can not distinguish that it is even present. But sometimes those 1-20 base pairs are different. The fallacious assumption that all changes in mtDNA are due to mutations in the mother is completely off. The differences between mother and child are almost always due to the father's contribution, and not to mutations. This has serious consequences for branch dating based on mutation rates.

> undiscovered checksum scheme

I don't think checksum is a fair metaphor for anything happening in biological systems.

> Most mtDNA between humans is the same

And most DNA is also the same. A percent difference is the kind of thing that would require millions of years of divergence to develop.

> mtDNA is only 16,569 base pairs long

This is really not so precise. There will be a mixture of lengths due to insertions and deletions, even in the same individual, even in the same cell.

> The differences between mother and child are almost always due to the father's contribution, and not to mutations.

Do you have a citation for this?

Checksum is a solid analogy, take natural abortion. If a fetus fails specific challenges it’s removed. This is very common, with a significant portion of pregnancy’s ending this way.

The number of base pairs in human mtDNA is not a subject of scientific ignorance nor of dispute; it has been known for decades. [1] This kind of objection is unproductive, and indicates one may benefit from personal study of the subject instead of arbitrarily casting doubt.

[1] Sequence and organization of the human mitochondrial genome (1981). https://www.nature.com/articles/290457a0

The big number of mitocondrias inherited form the mother and the small number of mitocondrias inherited form the father don't mix to become a single time of average mitochondria. Each mitochondria lives happily independently, and each one reproduces by asexual division making a copy of its genome.

Even if you assume that the 100% of the mitochondria comes from the mother, there are well known cases of mother that have a mix of normal and defective mitochondria and the children have a similar mix of normal and defective mitochondria. In this case the variation of the proportion of the normal and defective mitochondria between the mother and the children can cause that some of them get a worse version of a desease.

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