I’m just going off of what I’ve read and what has been said. I’ll be growing it myself to find out.
And if as it’s said, environmental factors play a role in male vs female flowers, I may even keep one Morris Burton potted in the driveway (also the greenhouse as applicable once built) to see if I can microclimate it to a “zone 7/8” tree to see if it throws any male flowers.
Persimmon sexuality is governed by the OGI and MEGI genes - basically an epigenetically controlled mechanism. The expression of dioecious flowering is controlled by methylation patterns of these genes which in is mediated by ethylene. It is suspected that the environmental effects that sometimes induce sexual fluidity in persimmons is due to the fact that persimmon is polyploid and can have multiple copies of these genes each with their own epigenetic imprint and the environmental effects could cause some change in the methylation patterns - possibly due to interference with the ethylene messaging. I think the Japanese scientist responsible for this insightful research is named Akagi. Next year, I plan on messing around with ethylene inhibitors on my trees to see if I can force any of my females to sport some male flowers. One side effect, of using two females for crosses is that all progeny are also female so no having to grow out non-fruiting progeny.
I have 3 Morris Burton trees now for 14 years and never notice a male flower on any of these trees. Meader and Early Golden had male flowers on occasion.
What is the astringency of your MBs? Do they turn non-astringent early enough to be similar to J-PCNA kakis (i.e., you can eat them firm)? Or do they turn non-astringent when fully ripe but not mushy? Or do they need to be super-over-ripe and gooey like many other DVs?
Ok, so my middle scenario – “when fully ripe but not mushy.”
That means that I have to temper my expectations. With current genetics, Morris Burton is not NA like a J-PCNA or even C-PCNA kaki. It’s more like a moderate-astringency PCA that doesn’t need to be over-ripe.
In turn, that implies that a MB x any other DV cross will not produce NA offspring. Such a cross would probably only dilute whatever is happening in Morris Brown.
Maybe the initial step should be to cross MB with itself, hoping that some offspring will concentrate whatever genes may be responsible for its low astringency. MB progeny may never be truly NA but maybe the astringency can be low enough to ensure non-astringency early in the ripening process.
At this point we don’t know whether any reduced astringency in a ripe Morris Burton is due to (1) low production of astringent compounds followed by dilution, or (2) early binding/precipitation of astringent compounds by acetaldehyde.
In another thread, @Fusion_Power writes: << There are some things known about Morris Burton that could be very important. It is lighter colored, more yellow than orange. >>
Based on this observation and a presumed connection or overlap among the biopaths for astringency and coloration, he suggests that Morris Burton may be a good candidate for breeding efforts to produce a NA variety.
However:
The pictures posted above by @parkwaydrive seem typically orange.
And @tonyOmahaz5 writes, “Morris Burton fruits . . . had no Astringency when turned real reddish color and soft to squeeze. . . .” So Tony gets fruit that are red. I get that the difference between red and orange is somewhat semantic (people define colors differently), but it’s a fair distance from red to yellow.
Does anyone else get yellow fruit from a tree supposed to be Morris Burton?
Morris Burton is probably a recessive trait which suggests it will pass on the trait, but it will be covered up by normal dominant genes. This is not proven. Solid evidence from other low astringency varieties suggests it is always recessive. F2 crosses should be able to recover the traits at about 1% of offspring. An F1 backcross to Morris Burton would be a good option with about 3% showing the trait.
There appear to be 3 different mechanisms associated with low astringency. This is an educated guess meaning I can’t prove the mechanism for Morris Burton. Given that the tannin biopath is several hundred steps with probably 10 to 20 regulatory genes, there is a lot of room for more genes that reduce astringency. Keep in mind that astringency is the plant protecting seed until they are mature at which time the astringency drops so the seed will be dispersed by animals.
Reduced production of astringent compounds - PCNA
Accelerated binding of astringency compounds during ripening - PVNA
Non-accumulation of astringency compounds, they are produced but do not stay around in the fruit - Morris Burton
PCNA is a result of significantly reduced production of astringency compounds early in fruit development, so that fruit can be eaten even if unripe.
PVNA is accelerated binding of astringency compounds in the presence of seeds, presumably due to the production of acetaldehyde either by the seeds or by the flesh in response to the seeds. It is pollination variance.
I don’t think we have any idea what is happening in Morris Burton. What evidence is there for an assertion that astringency compounds “do not stay around”? And what supposedly makes them go away?
After a little research (most reported above), I’m worried that Morris Burton may be over-hyped. Note that based on the testimony above from people who actually grow it (!), Morris Burton appears to behave like other DV varieties.
Tony gives what may be the most authoritative testimony after 14 years – non-astringency when really ripe. That’s great to know, and it puts Morris Burton on a par with a few other great varieties. But it is not really special.
It’s quite possible if you pay close attention. I haven’t heard anyone claiming they’ve seen them on H-63A, but that could just be that most people either don’t know what they look like or aren’t really looking since it is probably a small group of people like us who have a use for them. In my experience, the male branchlets (on my Early Golden) don’t appear every year, and they tend to be pretty small weak branches for some reason. I know J.C. McDaniel from the University of Illinois tried grafting the male branches to rootstock back in the 50’s and 60’s, but they always reverted back to female.
I’m already growing H65A, which is Morris Burton x Early Golden. As noted elsewhere, Early Golden family trees tend to produce male flowers. So I have some hope that H65A may produce some male flowers.
I’ve ordered scions of Morris Burton, which I will graft onto seedling rootstock and onto my mature Prok tree. As noted above, there is some testimony that Morris Burton may also produce some male flowers.
So I will grow both. When and if I see male flowers, I’ll attempt some cross-fertilization. If I never see male flowers, I’ll have to be content just to eat the fruit.
– If the male flowers are on H63A, then any offspring will be 75% Morris Burton (1/2 x 100% + 1/2 x 50%).
– If the male flowers are on Morris Burton, then I’ll attempt some crosses of MB with itself. Any offspring will be 100% Morris Burton but with different assortments of the MB genome.
If there is ANY genetic tendency in Morris Burton to non-astringency, maybe one of these offspring will win the genetic lottery and concentrate multiple copies of the non-astringency genes.
Re Luo Tian Tian Shi – Thanks. But did you intend this as good news or bad? Here, a tree that breaks bud before early May is vulnerable to freeze. For example, this coming Saturday morning (2 days away) is forecasted to be below 0 F.
