It’s name is just outdated a little, similar to ‘Early’ in Early Golden. It’s described as large fruited mid season with high productivity. Unfortunately Gerardi don’t described each cultivar in the same way but it should be later than EG. I don’t find more details about it’s origin other than the introduction in the end of XIX century.
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I have seen his conference papers cited
- American persimmon varieties and their desirability
- Persimmon varieties and propagation
If you have electronic copies, please upload them 
It’s look like it’s only available to ‘Persimmon World’ group members. I don’t own this photos so I couldn’t uplode them (American persimmon varieties and their desirability).
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This is a little off topic, sorry. Please tell me if this makes sense:
The J-PCNA mutation occurred long ago. As it is recessive, for a long time it would have been masked. But for some reason, the allele must have managed to spread. Eventually the recessive allele was present in all 6 chromosomes in some trees. Presumably, one or more of these trees was discovered and domesticated. As some PCNA varieties bear male flowers, these male-flowering trees could have been used in breeding. The existence of male-flowering full PCNAs would also have accelerated the spread of the PCNA gene in the wild.
Why did the recessive PCNA allele spread? Could it have been adaptive in some way, even though recessive and unexpressed? Or linked to some other adaptive gene(s)?
Doesn’t this scenario imply that the PCNA allele is fairly widespread (but masked) in the wild Kaki population, at least in the region of Japan where PCNA Kakis originated?
If this discussion gets more than a few posts long, I’ll start a new thread.
It was not necessarily adaptive in climate terms. Sometimes a gene changes desirability of the fruit which means the seed are spread more often, in this case probably by man.
A statement like this could be mostly true but fail. For example “fairly widespread” is probably not true. Recessive genes tend to find their way into a population where they remain at a very low level until eventually paired with enough similar or identical recessives to be fully expressed. An exception occurs when a recessive gene conveys a survival advantage. A classic example occurs in humans where a single copy of the sickle cell gene gives a huge advantage in surviving mosquito spread diseases. When both copies are for sickle cell, the disease is fully expressed resulting in a survival disadvantage.
Maybe I don’t understand what “recessive” means. I assumed that a sole “recessive” allele is totally masked – no impact. But in both of these examples, you’re assuming that the recessive gene has an impact. In the first example, the “recessive” gene is changing “desirability” even though it does not create non-astringency. In the second example, the single gene is providing protection against malaria but it doesn’t cause anemia.
Is that right – the recessive allele has subtle effects even when paired with a dominant allele or alleles?
Edit: I’ve done some further reading, which indicates that a sole recessive allele may have various impacts on the organism. So my follow-up questions are: Do we know whether the PCNA allele is present in some named PCA Kaki varieties? Do we know whether the presence of a PCNA allele (or alleles) has any observable impact on fruit quality (or anything else)?
It could also be closely linked to a trait that does have a major impact on survivability too
Recessive genes often are expressed which can be described as being “penetrant” meaning the trait is much less observable but still has an effect. A fully recessive allele causes no observable changes.
A recessive that is penetrant is expressed in varying levels depending on what the gene does. Using an example, some genes regulate production of a protein. If 2 functional copies are present, both trigger expression of the protein. If 1 copy is present and 1 dysfunctional gene is paired with it, the usual result is production of the protein - usually at reduced levels - by the functional gene. If both genes are dysfunctional, no protein is produced. Several known genetic diseases work like this. This gene would be referred to as penetrant because it results in lower production of the protein.
Another variation would be the classic red pea crossed with a white pea which produces a pea with pink flowers. Even though red is dominant and white is recessive, the expression is “penetrant” because the flowers are pink, not red.
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@Phlogopite @jrd51 @Fusion_power
Present day genetics treats PCNA as one of many variants caused by the divergence from dioecy. As Ross points out, the survivability of this trait is likely due to ecological pressure. Darrel continues to push old-school ideas about a recessive gene. I’ll again point out that there are many genes involved in a cascade of messaging to build a fruit. Somewhere in there NA is tripped for construction – which may be due to the interaction of several genes. Further, genes need not be binary switches – a fact noted in studies of the AGAMOUS class genes in plants. Whether or not all ploidy strands need to express the NA trait in an individual is pure speculation. We won’t begin to unravel (literally) this detail until advanced sequencing tools are developed.
Nice to see Jerry’s own evaluation notes.
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Interesting to see that I-94 / Valeene Beauty has only “average” taste. That seems to contradict the ratings in Claypool’s notes.
Actually, it emphasizes the difference in cultivation locations.
Maybe we can say (1) it contradicts Claypool’s notes, and (2) the difference might be due to location? But perhaps you can explain what you mean. I thought that both Claypool and Lehman grew persimmons in Indiana.
@jrd51
Let’s begin with the copy of J. Lehman’s notes posted by Dax – which you pointed me to a few days ago. At the bottom, Jerry says:
I’m often asked which is the best tasting. Taste is subjective. What may be
best for my self, others may not judge as best. If it isn’t good here in
Indiana it isn’t distributed.
Next, about J. Lehman and J. Claypool living in the same state. According to Google Maps, Lehman’s farm in Terre Haute IN is 90 aerial miles ENE of Claypool’s property in St. Elmo IL. Now consider the climate 90 aerial miles west of you.
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That would put me in New Haven CT, close to where I grew up. Growing conditions there are nearly identical to here.
I get that 90 miles can matter sometimes. 90 miles west would put you in the Pacific; 90 miles east would put me in the Atlantic. But it seems to me that 90 miles at roughly the same latitude on flat land in Indiana (or southern New England) don’t matter much. For that matter, most forum members would probably assume that 1000 miles don’t matter if the growing zone and growing season are similar.
In a recent thread on this forum, people made a big deal of Claypool’s ratings of Valeene Beauty and a sibling. Were those ratings useless? We’d all acknowledge that taste is subjective. But what about growing conditions? What are the limits on our ability to generalize from reports by growers who are 10 . . . 100 . . . 1000 miles away? Surely distance is in any case a poor guide.
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If you are in Providence, it puts you in Torrington, CT.
Well, the point holds for ANYWHERE in southern or central CT. You don’t need to make assumptions about where I live.
But to be precise, I live in Bristol RI and I grew up in Fairfield CT, which is 85 miles away as the crow flies and slightly south of west. And growing conditions are nearly identical.
But seriously, isn’t this a quibble, distracting from the substantive question?