As far as I know, you are right that ethanol / acetaldehyde from PV seeds is responsible for the de-astringency and the brown color. My recollection is that the seeds produce ethanol and the flesh changes the ethanol into acetaldehyde, but please correct me if I have that wrong. Moreover I believe that the amount of ethanol produced by the seeds is dependent on the number of PV genes. So the gene impact is somewhat additive.
Meanwhile, I have been thinking along similar lines as you in #1-3 above, though you articulated the issues better than I could. Given a caveat that hybridizing species is always a crap-shoot, these issues have led me to worry that breeding a non-astringent PVNA Kaki x DV hybrid may require overcoming these obstacles. At minimum that would seem to imply a need for more PVNA genes in the hybrid than in a pure Kaki. Again, very speculative.
One item to add. DV seems to have at least one other mechanism that reduces tannins. jPCNA is from down-regulation of Myb4. cPCNAās have some form of up-regulation of Myb14. An unknown but similar effect, likely another Myb?, causes varieties such as Morris Burton to have reduced astringency.
Pure speculation, but it looks like combining all three sets of genetics could totally re-write the persimmon astringency paradigm. It will take targeted genetic tests to ever achieve. āJust breeding persimmonsā without a method to track the genes would be an exercise in futility. Hexaploid genome, 3 different but potentially complementary genes at least 2 of which are recessive, and relatively long generation times suggest it could be done in about 12 years with genetic tests but would take many lifetimes otherwise.
We need know more about this. Iāve read such reports before, and I ordered scions of Morris Burton to graft this spring so that I could try it out. But the story seems to come and go. Iād expect a lot more excitement about the variety and about potential crosses with other DV names if it were observed reliably.
Do we know whether Morris Burton always loses astringency early? Does the loss depend on any known or possible environmental conditions, such as hot weather?
Anyway, my basic point is that if early loss of astringency in Morris Burton is reliable, we should be paying much more attention.
There are some things known about Morris Burton that could be very important. It is lighter colored, more yellow than orange. This indicates a change in the carotenoid biopath. The second is lowered astringency though I donāt know enough about it to say if the astringency is lost when fully ripe or if it is lost earlier in fruit development. The change to yellower color indicates the Beta Carotene step is interrupted somewhere much earlier in the sequence, maybe at phytoene. This is the step where tomatoes have more of a yellow/tangerine color. Perhaps not the same in persimmon, but it is intriguing to speculate.
You could almost put together a breeding plan where a cross involving Morris Burton, DV X DK hybrids, and cPCNA would result in a cold tolerant fruit that never develops astringency. It could be eaten any time the fruit got sweet but probably would be best when mature ripe. This would not require PV genetics because the tannin biopath would be disrupted at 3 stages before tannins form. Add in a requirement for large (apple size) fruit and you can see commercial potential.
If it were a white persimmon, I would be concerned about flavor. Since it is a yellow persimmon and I know of plenty of good flavored yellow fruits, I donāt think it will be a problem. This is just a guess and needs empirical proof.
I only have detailed knowledge about flavonoids from tomato, however, the biopaths involved are highly conserved in fruiting plants so it is likely similar in persimmon. There are over 400 known flavor compounds in tomato most of which are produced in the carotene and anthocyanin biopaths. One gene prevents accumulation of anthocyanins. One known gene shifts skin color from yellow to translucent along the way whacking a huge number of flavor compounds. Extending this to persimmon suggests there are hundreds of compounds in persimmon most of which can be increased or decreased.
Sugar/sweet - arguably the most important, part of the starch biopath
Acidity - probably second most important, part of the alkyl biopath (related to starch)
Color - primarily from carotene and anthocyanin biopaths
Umami - the unique flavor compounds our taste buds sense, hundreds of compounds involved
This begs a question why flavonoid biopaths are highly conserved. There are two closely related reasons. The first is that many flavor compounds do double duty protecting the plant from intense sun, pests, and diseases. The second is that getting seed spread is crucial for plant survival therefore attracting something to eat the fruit and spread the seed is a key trait. We can track these traits across many genera which infers the traits have been around for 10ās of millions of years.
Iāve seen studies where the peak in tannins occurs before growth rate picks up and other studies where it peaks after. Itās difficult to monitor changes in both traits with enough precision. I donāt think it really matters in medium to large fruited cultivars though. The increase in fruit size is so great after tannin production shuts down in Japanese NA cultivars that whether it started with a high or low concentration of tannins becomes insignificant.
Acetaldehyde can be produced from ethanol as part of normal ethanol metabolism, just like in humans, or it can be produced from pyruvate. I believe genes from this second mechanism are upregulated in PVNA and Chinese PCNA cultivars. Post-harvest removal of astringency in persimmons makes use of the first mechanism.
A quick look at the table from this paper shows at least 8 compounds involved in persimmon flavor that can be derived from early steps of the flavonoid pathway. So yes, itās possible that downregulating the pathway could impact flavor. However, there are multiple ways to get to these compounds, and itās important to keep in mind that tannin biosynthesis uses the same starting molecules and potentially competes with the biosynthesis of some of these flavor compounds. So we really canāt say what the impact will be. In tomatoes, it seems that a lot of the monoterpenoids important for flavor come from the carotenoid pathway. Other plants have a dedicated monoterpene pathway. Persimmons donāt appear to have a lot of monoterpenes or norsioprenoids, the other aroma compound class that comes from carotenoids, so who knows.
I get the argument that plants evolve fruits that will be eaten to encourage seed dispersal, but probably itās a two-way street. So the taste buds of animals evolved to find the chemical compounds that are useful to them flavorful. For example, two major sources of calories ā sugars and fats ā are very tasty. Ditto salt. Maybe flavor in fruits and vegetables is a proxy for vitamins, minerals, antioxidants, essential fatty acids, etc.
Thanks again. Your reward for more information is more questions.
The excerpted quote clarifies the PVNA process for me. Do you know where in the seed these reactions take place? Is it purely maternal tissue? Iāve wondered whether genes brought to the tree by the pollen can have a role. And does the acetaldehyde move into the flesh by an active or passive process?
Related to flavor, at least one of our members has said it is excellent, along with Lena and H63A and a few othersā¦ I trust those reviews from @Barkslip especially, because he has tasted so many different varieties.
Where Iām going with that, is that if color change is an important indicator for particular ripening /taste /astringency related traits @Fusion_power, I would surmise that Morris Burton may be a path to maintain excellent flavor.
I hope to add my input in a couple years if my grafting is successful this spring.
Which is why I used Morris Burton as an example above. It is highly likely a larger fruited Morris Burton offspring could set a new flavor and fruit production standard for persimmons.
Unfortunately thereās not a lot of recent information on PVNAs, and the few papers I found were paywalled.
For Chinese PCNA cultivars I think itās pretty clear that the reactions occur in the fruit pulp.
For PVNA cultivars, I donāt think we can say if the seed is producing ethanol/acetaldehyde or if the pulp is triggered to produce ethanol/acetaldehyde by the presence of seeds. Both ethanol and acetaldehyde are extremely soluble in fruit tissues and have no problem crossing cell walls or seed coats. The fact that tannin precipitation and ethanol/acetaldehyde concentrations are higher in the flesh surrounding seeds doesnāt tell us that it was the seeds that produced the compounds.
I wouldnāt get too hung up on the often-repeated āPVNA seeds produce ethanolā fact either. As far as I can tell, no one has followed up on the studies done in the 70s and 80s on PVNA persimmons. Just because they measured ethanol doesnāt mean that acetaldehyde isnāt the main molecule we should be concerned about. The enzymes work in both directions, and acetaldehyde is much more toxic than ethanol. Itās possible that whatever acetaldehyde doesnāt immediately react with tannins gets turned into ethanol to limit toxicity.
That said, ADH and PDC genes, the ones responsible for converting ethanol and pyruvate to acetaldehyde and back, are upregulated in the presence of abscisic acid in many plants. Abscisic acid is produced in seeds to induce embryo dormancy. I wonder if this may be the actual underlying mechanism for tannin precipitation in pollinated PVNA fruits.
I realize I oversimplified the mechanism behind the treatment methods to remove astringency in persimmons. It seems that the pyruvate to acetaldehyde pathway is induced as well in methods that deprive the fruit of oxygen.
My only issue is the paragraph quoted immediately above. PVNA is a trait of some persimmons. Some others are PVA (which is like PVNA-lite). Most are just PCA. Presumably abscisic acid is produced by all persimmon seeds. Are you guessing that some varieties produce way more than others?
Whether this specific idea works or not, I like the general idea that seeds in PVNA fruit donāt produce ethanol or pyruvate themselves but rather they produce a substance that induces the flesh to produce one or both of those compounds.
Coincidentally, Iām planning to add Morris Burton too. Iāve already got H63-A, Barbraās Blush, and Dollywood. Does anyone know if any of them produces pollen (e.g., male flowers)?
LOL, I guess weāve drifted a long way from Ukraine!
Do we know if it [produces any pollen (e.g. male flowers)?
Don Compton has a bunch of Morris Burton crosses growing in his orchard from seed he got from James Claypool when James got too elderly to continue. They would have been row M in the Claypool orchard.
Just happened upon this thread and maybe it is a bit late to react to your original question but I can confirm that Gora Roman Kosh is indeed PVNA. Actually I had always assumed that it was PCA so I never bothered to try and eat some fruit fresh from the tree. Last season I noticed that that the flesh from a soft fruit was a darker color like the seeded PVNA types so I tried to eat one fresh from the tree and it was indeed non astringent. I have a lot of pollinator varietes in my orchard so all my persimmons are well seededā¦
According to what is reported above, Gora Roman Kosh is an open-pollinated cross of Nikitaās Gift. Do we know whether any PVNA persimmons, which often bear male flowers, have been used in Ukrainian breeding?
I ask because this observation suggests the possibility that the Kaki PVNA allele can produce seeds that remove the astringency from a hybrid with virginiana parentage. This has never been demonstrated before, as far as I know. It seems a quick route to non-astringent hybrids. A non-astringent PCNA hybrid would need to have 6 NA alleles. A non-astringent PVNA hybrid would need to have only 2 PV alleles.
[I make this final assertion because my reading of the results of PVNA breeding experiments suggests that 1 PVNA allele produces a PVA type, whereas 2 or more PVNA alleles produce a full PVNA type.]
Has anyone else crossed Nikitaās Gift (or other hybrid) with a PVNA Kaki as pollen donor?
Just checked with Dax regarding Stan observation on his Gora Roman Kosh being Nonastringent. Stan said the bird may have pecked the fruit and it ripened nonastringent on the tree that year. He then tested taste the fruit last year and again this year straight out of the tree and they were astringent. So it may not be PVNA and needed more observation. Oh well.
