I saw your post there and wrote my opinion about this topic but then I thought about something. Maybe Jerry made a misstake when he send the material ? For example he labeled some Rossyanka seedling as MB ?
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This is always possible but if Jerry Lehman mistakenly sent Rosseyanka, which is 50% Kaki, wouldn’t the researcher have reported something like, “MB shares half its alleles with kaki!!!” Or “MB shares at least half the alleles that we tested”?
First of all I should wrote instead about JT-?? or it’s seedling as it would have non astringent gene from Taishu.
As I studied everything in this paper again there is a least a few inaccuracies :
- Electrophoresis for my knowlage only work as a method of DNA fragmentation, and not identify each allel.
- I couldn’t find any information about Dr. Sakar (any research result etc.)
- D kaki and D virginiana don’t cross without embryo rescue (first in 1958) so how could we see introgression in a cultivar found in 1955 ?
- If allel A develop in population 1 the same allel wouldn’t appear in population B, similar trait would be conected with allel B.
- If MB is the only source of NA gene in each of crosses we should get plants with this trate (dominant gene). If this gene is recessive non of Claypool’s trees will inherit a recessive homozygote.
Yeah, all great points.
Re #4: Since DK and DV are both members of the Diospyros genus, I suppose they could share alleles from an ancient common. ancestor. That’s assuming no mutations in the interim. But probably all / most Americans would have the same allele. And it’d have nothing to do with astringency.
Your point – similar trait, different allele – is displayed in Japanese and Chinese non-astringent persimmons (J-PCNA and C-PCNA respectively), which have different mechanisms for achieving non-astringency.
Also, it seems that strategies for removing astringency from Kakis (e.g., CO2, ethanol) don’t work in Americans. This seems to suggest some difference in the metabolic processes that create astringency in the two species.
Re #5: The allele that produces non-astringency in Kakis is known to be recessive. So no cross between variety having this allele and a variety not having it could produce a non-astringent offspring. What this means is that even if MB has the same allele for non-astringency as the Kaki J-PCNAs, its MB x DV offspring could still never be non-astringent.
The allele in Kaki C-PCNAs is known to be dominant. If MB shared this allele, MB itself would already be non-astringent when unripe, which is isn’t.
p.s. JT-02 presumably has 3 (out of 6) alleles for non-astringency, inherited from Taishuu. Elsewhere I’ve recommended back-crossing JT-02 with any male-flowering J-PCNA (e.g., Taishu, Hanagosho) to produce a non-astringent hybrid.
#4 I was focused on ‘astrignecy locus’ in this point. In my theory this locus have at least 2 different allels in 90n american persimmon. Allel A - ‘normal’ gene (dead soft fruits are edible) , allel a - early loose of astringency (sources MB, EG, Piepher, likly all 3 have different variants like a1 , a2 , a3 which work like co-dominant genes). Why I think that way ? Some cultivars like Geneva Red, Prok, EG, MB, L-crosses mentioned above have been reported as loosing astringency faster. If my knowledge about their peigree is correct EG is or could be involved in all of them (in various ways). Maybe someone could tell me if same thing appear in Claypool’s MB x EG ?
About the rest of their genepool it’s highly possible that they share a lot of allels e.g.for sex determination.
What I noticed from this fruit was I picked one that seemed fairly ripe from the tree and it had no astringency. Braver, I picked one that clearly appeared less ripe and ate it. No astringency. Does it lose astringency better or does it hold on to its fruit longer? Idk. There was a third fruit on the young tree which forgot about and it was gone by the time I returned to the tree days later.
Some varieties I am not afraid to gobble up once they hit the ground. Some (or many) are on the definite “caution” list here (e.g., 100-45, Osage, …)
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Sure, it seems very likely to me that production of tannins in American varieties varies under genetic control that is quantitative, by which I mean that each gene may have some allele(s) that result(s) in more tannins, some that result in less; and, of course, the genotype can range from 6 high tannin alleles to 6 low tannin alleles and everything in between. And maybe more than one allele is involved.
In contrast, the Japanese kaki Astringency allele appears to be all or none. A persimmon with 0 Astringency alleles (i.e., 6 NA alleles) never produces much tannin. But persimmon with just 1 Astringency allele produces lots of tannin. Obviously this is different than the proposed (above) American model.
Actually, it is a concept left over from R. Fisher’s theory of genetical variance – which no longer applies to our modern understanding of genetics. “Trait” is more accurate than “allele”.
I completely with you that the appearance of a D. kaki trait in Morris Burton has no relevance to the discussion.
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