Question about Ukrainian persimmon breeding

A female DV is the only way to have confidence in both parents. A male DV offers no hint at fruit quality.

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All this talk about genetics and the way chromosomes interact reminds me that chromosomes often swap entire sections or a section will separate from its normal location and glom onto the end of a different chromosome. The necessary genes are still there, but it gets dicey during meiosis when gametes are formed. In some cases, an abbreviated chromosome winds up in a reproductive cell which is a problem because the paired chromosome from the other parent is normal.

Sometimes viruses get into the mix. A section of virus DNA wound up in chickens on chromosome 1. The result is blue eggs. Similar things happen when mycoplasma invade plant cells.

Then there are the outre things that can happen. An entire genome may duplicate resulting in a tetraploid plant. That doesn’t usually last more than a few hundred generations before the genome either sheds chromosomes or more likely repurposes bits and pieces so the entire thing still works but now we describe the previous tetraploid as a diploid.

And you have to remember the possibility of different but related species crossing. The Triangle of Wu describes this in context of brassicas where two related species crossed and produced rutabagas. The rutabaga basically has the entire genome of a cabbage and the entire genome of a turnip.

Ain’t genetics fun!

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OK, I caused confusion by saying male/female where I really meant pollen donor/recipient. Obviously a variety that produces only male flowers can never produce fruit, hence your point.

I’m not sure why this issue applies only to Virginiana, however. A pure male (no fruit) would be a difficult choice whether Virginiana or Kaki.

On the Kaki side, there are lots of varieties that produce both male flowers and female, at some time or other, under some circumstances or other. Taishu is a good example. It produces high quality PCNA fruit but if also makes male flowers and serves as a pollen donor in many crosses. So it can act as the “male” (i.e., pollen donor) in a cross because it also is a “female” (i.e., produces fruit). In such as case, male flowers don’t imply no fruit. So we can evaluate the fruit.

On the Virginiana side, honestly I’m less sure how sex works but I know that there are some varieties that produce both female and male flowers (fruit and pollen). I have also read that some varieties may produce all/mostly male flowers when young, then all/mostly female flowers when old. Again such a variety could be used rationally as a pollen donor because sooner or later we can assess the fruit.

Next, I understand that persimmons often produce hermaphroditic flowers, along with female and maybe male flowers. I suppose that these hermaphroditic flowers could also serve as a source of pollen in a fruiting variety.

Finally, it is possible that a DV cultivar could be selected as a pollen donor for reasons that have nothing to do with the fruit. For example, we might use a pure DV male as a pollen donor if it were extremely cold hardy. Fruit-wise, we might just hope for the best. If this sounds too crazy, I’d point out that male figs (caprifigs) produce inedible fruit. ALL fig crosses involve a fruit-less pollen donor.

Anyway, I appreciate that the table may be tilted in flavor of the DV variety as the female. I just didn’t want to jump to that conclusion.

p.s. I believe that there is a convention that the cross should be described FEMALE x MALE. Most persimmon crosses that I see are ordered this way. In the article referenced above, Rossiyanka is described as DV x DK, which would imply a DV female. But Hybrid F 1648 is described as DK x DV, which may imply that DV can also serve as pollen donor. Or it can just be sloppiness.

Your timing on bringing up the blue eggs is fortuitous. A coworker brought in an Emu egg from the farm he is now renting at and we were discussing all the colors chicken eggs could be. Not to derail the thread, but I figured I’d mention it in passing.

Nine to be exact though you have to factor in that there are varying shades of each color. It is not an exact thing. This is relevant in a way to the thread context. All chicken eggs start out with a calcium based shell that is basically cream in color. Some chickens have additional genes that make the shell intense white. When the oocyanin gene is present, the cream/white shell incorporates bilirubin which produces shades of blue. If the porphyrin genes are present, the egg shell is coated with porphyrin which can give shades of tan, sandy, light brown, brown, dark brown, and too much brown (Cuckoo Marans). Then there are a few breeds that coat the egg with a pale pink layer. Combine some of the colors such as blue with brown and you get olive shades. Combine pink with oocyanin and porphyrin and you get spearmint green. How is this relevant to persimmons? The caroteinoid biopath is highly conserved and present in almost all fruit producing plants. This gives the orange color to persimmons, red, green, yellow, and orange to tomatoes (black tomatoes are on the anthocyanin biopath), and a few other colors and variations depending on the plant. It is possible we could find a white persimmon where the caroteinoid biopath is disruped in all 6 chromosomes. When thinking about a PCNA persimmon, there is a strong tendency to think of this as a “gene”. In reality, it is a biopath with variations of expression. If the biopath is interrupted, the result is a PCNA fruit. When I started thinking of genetics in terms of “biopaths” is when genetics started making sense. I once wrote an entire post on tomatoville about the caroteinoid biopath taking the chemical expression step by step from precursors to phytoene to protolyocopene to lycopene and then to the final step for beta carotene.

From reading the above, you might think the porphyrin genes are only present in some chickens. WRONG! The genes to produce porphyrin are present in all chickens, but in some chicken breeds, they are turned off. Realizing this was a watershed moment in my efforts to breed blue egg laying silver laced wyandottes. Now think of this in context of PCNA persimmons. All evidence I’ve seen so far is that some varieties have the astringency genes turned off. The biopath is present in all persimmons, but it can be disabled!


@parkwaydrive – John, here’s a list of 15 DV varieties grown in Ukraine, referenced in the article attached below. I’m not expert on DV sex, but I’m pretty sure that both Szukis and Early Golden have male flowers and could serve as pollen donors. The only one I’ve grown is Prok, which seems a pure female.

<< John Rick, Meader, Weber, Prok, Yates, Szukis, Supersweet, Pieper, NC 10, Hess, Geneva Long, Garretson, Evelyn, Dickie, Early Golden >>

2_2_2018.pdf (825.8 KB)

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This got me thinking about the nature of the interruption in PCNA persimmons. Here’s some info regarding C-PCNAs. The excerpt is from the article linked.

As I understand it, destringency in CPNA involves primarily the down-regulation of a proanthocyanidin (i.e., PA) “biopath” at a point during fruit development, as well as other changes that render the PA more insoluble.

None of this detail alters what we know about the heritability of the C-PCNA astringency trait. The authors state, “The characteristic of losing astringency in J-PCNA and C-PCNA persimmon is genetically controlled by a recessive and a dominant allele, respectively.”

<< C‐PCNA persimmon originates in China. Its deastringency trait primarily depends on decreased PA biosynthesis and PA insolubilization at the late stage of fruit development. . . . . The expression of PA biosynthesis‐associated genes indicated that the down-regulation of the ANR gene at 140–160 DAF may be associated with PA biosynthesis and is decreased by inhibiting its precursor cis‐flavan‐3‐ols. We also found that a decrease in acetaldehyde metabolism‐associated ALDH genes and an increase in ADH and PDC genes might result in C‐PCNA persimmon PA insolubilization. . . . >>

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…Ahem… So after having a go at understanding this… I will try crossing the ones i have available (American/asian and hybrid/asian) As well as if whoever has a better understanding and does the proper crossing and is willing to send/sell seeds, I am willing to grow at least a few hundred additional seedling out. :slight_smile:


Good point. I was rolling in an assumption about the probabilities of access to those. F-100, Garretson, Killen, and Florence have also been shown to put out the occasional male branchlet. I had one on my Early Golden last year but the tent caterpillars decided to take out that branch. I think D-127 also fruited a time or two, but I think it may be extinct now as it is no longer in the Claypool orchard.

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@Fusion_power – Here’s some similar info regarding J-PCNAs. The excerpt is from the article attached.

<< The astringency of persimmon fruit is caused by proanthocyanidin (condensed tannins) located in the vacuoles of tannin cells, which are specialized cells for tannin accumulation within the fruit. In persimmons, partial DNA sequences of nine structural genes involved in tannin accumulation via the flavonoid biosynthetic pathway (Fig. 7), namely phenyl-alanine ammonia lyase, cinnamate-4-hydroxylase, 4-coumarate:coenzyme A ligase, chalcone synthase, chalcone isomerase, flavonone-3-hydroxylase, flavonoid-3′ hydroxylase, flavonoid-3′,5′-hydroxylase and dihydroflavonol reductase, were isolated by PCR using degenerate primers and their expression levels were analyzed (Ikegami et al. 2005a). A comparison of PCNA (‘Hanagosyo’ and ‘Suruga’) and non- PCNA (‘Kuramitsu’ and ‘Yokono’) cultivars revealed that the sudden termination of tannin accumulation in PCNA-type cultivars is due to termination of the transcription of all nine structural genes involved in condensed tannin biosynthesis at an early stage of persimmon fruit development (Ikegami et al. 2005a). >>

JJPS_1242-62.pdf (2.8 MB)

That just confirms that the regulatory genes are turned off in NA varieties. You don’t get an entire biopath to stop functioning without doing something to the gene(s) that turn the biopath on. It is essentially the same thing that happens with white tomatoes. The entire caroteinoid biopath is turned off which results in white tomatoes. There is something lost in tomatoes when caroteinoids are not produced. That something is flavor. White tomatoes are among the most bland and insipid that can be grown. I wonder if something similar might be true of the tannin biopath in persimmons?


This question just brings my thoughts to further questions.

I would say it is safe to assume cPCNA, jPCNA, hybrid, and potentially virginiana varieties all have slightly different pathways to achieve removal of astringency.

This is evident to me in the thread discussing methods of removing astringency in some of the above mentioned.

So my questions then become, is it possible, or is it likely, that all of the above may share the same available mechanisms but may express those mechanisms differently, resulting in all the different types of astringency in the spectrum.

A lot depends. It is more likely that this is a single biopath which is present in all 6 copies of the genome. Since there are 6 copies, the same biopath expresses from each set. Now think of it as say 20 steps numbered 1 to 20. jPCNA interrupts the regulatory step so lets say it is step 1. DV varieties maybe work a bit different so lets say they interrupt step 4. cPCNA is a dominant gene so lets say it is step 21 that affects steps 1 to 20. If we cross a jPCNA X DV we get astringent offspring 100% because the recessive nature of jPCNA is overcome by the regulatory genes in DV. The same basic thing happens with jPCNA X cPCNA but with a quirk. Since cPCNA is dominant, at least some of the offspring should express cPCNA type NA. In a backcross to jPCNA, segregation should give about 3% that express jPCNA. This is just a bunch of speculation. Until we understand the tannin biopath and how it functions, we won’t know exactly what is happening with the genetics.

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This cross was done in this study. In this instance 22 of 34 offspring of C-PCNA x P-PCNA were non-astringent.

2327-9834-article-p371.pdf (507.8 KB)

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2/3 cPCNA in the offspring suggests it is most likely the cPCNA parent had at least 2 copies of the cPCNA gene.

This paper may have found the primary gene involved in turning on the flavonoid (tannin) biosynthetic pathway in persimmons:

MYB transcription factors regulate tannin and anthocyanin biosynthesis (among many other things) in most plants, and the pathway is pretty well conserved between plant species. In most cases, a mutation that disrupts the function of the MYB gene primarily responsible for a given pathway shuts down the entire thing. However, you can have multiple MYBs involved in regulating a pathway that get activated in different tissues (fruits vs leaves) or at different times of development (fruit set vs ripening). In grapes, two MYBs regulate anthocyanin production in the fruit, and both need to be mutated in order to get white grapes. Grapes are interesting because the two MYBs are mutated in different ways: one has a retrotransposon (aka “jumping gene”) inserted into the promoter region of the gene, preventing expression. The other gene has two point mutations that disrupt the function of the gene product.

The paper I linked suggests that DkMyb4 is the primary Myb regulating flavonoid biosynthesis in persimmon fruit, and their experiments found that the expression of this gene drops off dramatically in NA varieties shortly after flowering. This supports the highly recessive nature of Japanese-type NA, since even a single copy of whatever gene maintains DkMyb4 expression in astringent persimmons will be sufficient to turn on the flavonoid pathway. In my opinion, the fact that there is Myb4 expression early in development regardless of cultivar suggests that the mutation responsible is even further upstream in the regulation of the flavonoid pathway and not within the Myb4 gene itself. The tendency for some PCNA cultivars to maintain some astringency in some climates/growing seasons also supports this, and implies that certain conditions result in incomplete suppression of Myb4 expression. This probably isn’t all that important though, since it seems that astringency in Asian persimmons is definitely controlled by a single locus. Whether or not that involves one gene or many, they are close enough on the genome that they are inherited together.


Maybe going too far off topic here, but this is something I find super interesting. Carotenoids are broken down into a whole bunch of flavor compounds that are important not just in tomatoes but also watermelons, black tea, and wine.
Here’s a paper that goes into the parallel mutations in the carotenoid pathway of tomatoes and watermelons and how they affect flavor. Unfortunately it’s paywalled, but the summary is pretty informative.


I wonder whether the pathways for creating astringency differ materially in Kaki and Virginiana.

And if so, is it possible that the C-PCNA or J-PCNA mutation will have no impact on the expression of astringency in DV? Would a DV x K hybrid therefore have to inherit the Kaki gene(s) responsible for creating astringency before the Kaki gene(s) responsible for eliminating astringency could function as usual?

@GrapeNut – You had some great insights above. Any thoughts here? Thx.

Evolutionarily speaking, it would be unlikely that the two persimmon species have different biosynthetic pathways for producing proanthocyanidins (the type of tannin responsible for astringency in persimmons). I think most, if not all, plants use variations on the same pathway to produce these compounds. What we should expect to differ are the various regulatory systems for each step of the pathway, and as a result, the ultimate composition and concentration of the final products.

From what I have read, there appears to be two mechanisms for loss of astringency in Asian persimmons: dilution and precipitation. Dilution is simply the consequence of fruit development. Most of a fruit’s growth happens from cell expansion. Water is pumped into cells formed shortly after fertilization, causing them to swell. As water content increases, anything present in the cells decreases in concentration if biosynthesis doesn’t keep up. Dilution occurs in all D. kaki, NA and A, the difference being that in Japanese PCNA persimmons, the Myb4 gene mentioned above fails to be expressed and the tannins formed early on get diluted until they are no longer perceptible to us. On the other hand, astringent persimmons continue to pump out tannins at a rate that exceeds the dilution effect.
This paper found a correlation between cool temperatures after flowering, increased Myb4 expression, and consequently, higher tannin levels in PCNA cultivars. This suggests that the ast mutation affects Myb4 expression but isn’t on the gene itself and explains the phenomenon of astringency in PCNA cultivars grown in cool climates.

The precipitation mechanism is a bit more complicated. Tannins can only cause the astringent sensation if they are soluble. Under certain conditions, tannin molecules will bind to each other until they get so large they are no longer soluble and precipitate out of solution. This is (I think) the brown color in PVNA persimmons as well as the crud in the bottom of a red wine bottle. In persimmons, acetaldehyde molecules react with tannins, causing them to link together and precipitate. This occurs for astringent persimmons during the ripening process and for PVNAs slightly earlier.

The paper you linked above:
and this paper:
found that Chinese PCNAs have both mechanisms at work: some dilution due to reduced tannin production early on and increased acetaldehyde production prior to softening to precipitate the remaining tannins. It seems that another Myb gene, Myb14, both suppresses the tannin pathway (but doesn’t shut it off entirely) and upregulates genes that produce acetaldehyde. Because this would be a “gain of function” mutation that increases the effect of an existing gene, this may explain the dominant nature of inheritance. Myb14 should be present in all D. kaki, so the mutation likely affects how it is expressed.

To answer your question, if whatever gene is responsible for reduced D. kaki Myb4 expression can work on D. virginiana Myb4, there’s no reason why tannin production can’t be shut off early on, unless there are additional genes to switch on the pathway.

As for why methods to induce tannin precipitation don’t work in D. virginiana, I can think of three possible reasons. Purely speculative of course, and it’s possible the three work in concert:
1: The methods work, but without actually measuring the amount of insoluble vs soluble tannins, it’s impossible to know how well. It could be that American persimmons simply have too high of a concentration for the amount of acetaldehyde to completely neutralize. Simply tasting for astringency doesn’t really tell you how much is left.
2: American persimmons don’t produce a lot of acetaldehyde. I doubt anyone has measured the rate of loss of soluble tannins in American vs Asian persimmons. Could be that the process is a lot slower.
3. American persimmon genes for metabolizing acetaldehyde work more efficiently than Asian genes, reducing the effect on soluble tannins.


Thanks. It’ll take time to process.

Meanwhile one quibble, maybe a matter of emphasis not substance: As we all agree, prior to dilution per se, in PCNA persimmons there is a reduction in the rate of production of astringent compounds. So PCNAs benefit from both low production and then dilution.

I guess you imply this when you say “the Myb4 gene mentioned above fails to be expressed and the tannins formed early on get diluted until they are no longer perceptible to us.” It’s just that the “two mechanisms” you set up at the outset (dilution and precipitation) omit this down-regulation of the production process.