Re: Epigenome genetics

There is a lot of interesting information there that I will need to process at leasure, which I don't have right now.
However I do note artical on vernaliztion seems to have been outdated by more recent research on genetics of bloom/vernaliztion . There is a set of controlling genes called MADS-box that control blooming. There are two genes involved in control of vernalition plus vernaliztion gene itself. You may wish to look some of these studies up on www.scirus.com . Vernalization causes permanent change in the genetics. Any part of vernalized plant will produce a plant that acts as if it had undergone vernaliztion. ( I have mentioned this researach earlier) Thus there needs to be mechanism to reset these genes, otherwise ther wouldn't be a need for any furher vernaliztion. My speculation is a reversal by mother rhizome blooming. This would be similatr to lateral supression in tree growth. The terminal (top of tree) emits a chemical which travels down stem and slows growth of the lateral branches. If top of tee is cut there is now faster growth of the branches. We see some summer bloom in fall rebloomers wher mother rhizome failed t obloom in soring. For example, Blessed Again which bloomed for me severaal weeks ago whereas other fans mature enough are not reblooming, waiting for another signal.
This turning on and turning off and resetings fits with the epigenome theory.
This whole branch of genetics (epigenetics)will probably be clarified with time as has the MADS-box genes. There is a whole lot more, but not for today.
I'm becoming increasingly convinced that my everbloomers, such as Forever Blue, Blueberry Tart, Autumn Jester, Forever Violet etc, have as one of ther components, such fast spring growth that they bypass mother rhizome bloom supressor , or alternatly, increases are large enough in fall to undergo their own vernaliztion. In addition they have the genetics for Fall rebloom.
About 90% of genetic information in plant genes are non-active genetic material, most of it reflecting genetic evelutionary history. These are usually turned off through mythalization , but can be de-methylazied by stress factors. But this is random, not specifially tuned to enironmental stres placed on it.
At the same time there are some other specific responces to stress, such as the adaption to cold weather. Another whole interesting area of reseach. 

Chuck Chapman


Date: Sun, 31 Aug 2008 19:40:16 -0400 (EDT)
From: Paul Archer <pharcher@mindspring.com>
Subject: [iris] Epigenome genetics
I was watching "Nova" on PBS last night and their show "Ghost in Your Genes" got me thinking. It does somewhat follow what we are seeing in our Iris, although all particular instances of their discussion involves animals not plants. I will note that this information does not detract from the work we 
are doing as a group or by other Iris breeders.  It may simply help us
understand what is going on. Some ideas I had I will elaborate on later. They may be far beyond the scope of anything most people can fathom, but it is 
food for thought for those interested and indicates there might be some
advancements made toward our goals.
The show discussed what is called the Epigenome of DNA. This is the genetic material outside of the actual genes. This is the DNA that controls when a 
gene is turned on or off in an organism.
They discussed two issues. The first was differences in twins and how one twin can develop cancer or autism and the other be perfectly fine the cause being the differences in their Epigenome while their genes remain identical. The differences in the Epigenome are the presence or abscence methyl groups 
attached to the DNA that turn on or off the firing mechanism of the gene
itelf. Some human tests subjects are receiving chemotherapy of a previously discounted anticancer drug that was deemed too toxic. They are receiving it at much lower doses over longer time periods and it is killing (turning off genes in) cancer cells by removing the methyl groups attached to the DNA that 
made the cancer genes active.  This in effect makes the cells "reset"
themselves to a more natural state of activity.  The second issue they
discussed was that of generational inheritance. This is the inheritance of information in the DNA carried from one organism to another and then to the grand-offspring, a genetic memory. We inherit genes from our parents and grand parents but we also inherit their epigenome and how it was set at the 
time of conception.  The now documented evidence they have is that of a
isolated group in Sweden that went through famines and overabunances and then tracked the deaths and illnesses of their children and grandchildren. They 
found that even though the grandchildren didn't witness hardships or
overabundances they still fell ill although their grandparents expressed no such tendencies, particularly diabetes if the grandparental overabundances occurred. Similar experimental observations were made in mice with aggression tendencies relating to rearing habits of the mother mouse and the effects on 
her grandchildren with the grandchildren also being aggressive.

Here's a link to the page to see excerpts

http://www.pbs.org/wgbh/nova/genes/
NOVA | Ghost in Your Genes | PBS
So these two findings got me thinking how the epigenome might relate to Iris. 
You could have two (or more) plants of the same variety both at the same
apparent stage of development and one bloom and the other not. They are 
genetically identical but epigentically they are different.  Might there
simply be a way to coax the plants to have a similar Epigenome and "reset" it 
to our favor at the right time?

How does this effect the seed? We might have assumed that the genes are
"rejuvenated" once a seed is formed but now this may not be the case at all. Some gene are "rejuvenated" or shall we say in a juvenile/vegetative state and 
some are obviously probably not.  So what is actually carried over?
Would it be better to wait a few years to set seed on a newly received plant until it "resets" itself (if it can)? We have noticed some cultivars do take 
a few years to acclimate to a new climate and then they are fine.
How would the results be different in growth/rebloom in one year's batch of 
seed to a batch obtained years later from the same cross?
Might this also be a solution somewhere in there to those of us who try to grow rhizomes from another climate just to have them fail repeatedly either 
soon after transplanting or three years down the road just disappearing
altogether?
Is there some way we overcome the plant being epigenetically "set" by
chemically "resetting" its Epigenome to a base state as in the cancer
patients?
I'm not sure if Science knows just exactly what roles gibberellic acid and abscisic acid play in plant growth and dormancy, but we do know they do have a 
significant part.  Might these chemicals or other plant hormones be the
signals or actual culprits in DNA methylation/demethylation. I'll bet they do play a significant part. Could these or others chemicals be used to "reset" 
the Epigenomes of Iris?
Here's a link to a scientific article I googled that might shed some light. 
It does also show some epigentic inheritance (not genetic as we have
previously thought) of vernalization of seed from the parent. So our Iris may be affected in similar ways (dry, stressed summers vs. cool, wet ones). This may imply that a plant grown in a cold climate might be significantly more prone to produce cold climate rebloomers because the seed has been set that way, but not simply based on its actual genes, but it's Epigenome. Does this imply that the plants need to be "reset" before seed is obtained for your climate if your goal is to have warm climate rebloomers (and vice versa)? 

http://www.pnas.org/content/95/10/5824.full.pdf
5824.full.pdf (application/pdf Object)
I'm hoping Chuck will have some comments, some scientific insight and research 
reports he can scrounge up about all of this.


Paul Archer
Indianapolis, IN  Zone5

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