Genetics of fastigate growth?

Discussion in 'Plants: Science and Cultivation' started by sgbotsford, Sep 22, 2016.

  1. sgbotsford

    sgbotsford Active Member

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    Various mutations of common species exhibit columnar form much narrower than the normal form. From observation these skinny forms come in two flavours:

    A: Branch angle is decreased, making the branch closer to parallel with the source twig. Example: Parkland Pillar Asian Birch.
    B: Receptor for the growth hormones for apical dominance don't work. Every branch 'thinks' that it is the leader and hence heads straight up. Example Swedish Aspen.

    As a model of fastigate tree genetics would the following be reasonable:

    * The defective gene for either A or B is fairly scarce in the general population.
    * The defective gene is recessive.
    * Consequently the expression of the gene is fairly rare, as both parents have to be carriers.

    A colleague of mine proposed an alternative that fastigate trees are polygenetic -- It takes the right combination of multiple genes to exhibit the trait.

    Is there any way to tell in a particular case which model (or neither) is applicable?
     
  2. Daniel Mosquin

    Daniel Mosquin Renowned Contributor UBC Botanical Garden Forums Administrator Forums Moderator 10 Years

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    I'm drawing a blank on a search for fastigiation, and not much on a search for genetics and fastigiate. Did find this:

    from GENETICS OF ANGIOSPERM SHOOT APICAL MERISTEM DEVELOPMENT in Annual Review of Plant Biology

    That multiple mutations have been identified, suggests it is polygenetic to some extent,. That may not necessarily mean, though, that more than one gene need to devitate from the norm to exhibit the trait. Sometimes it could possibly be a single gene, sometimes multiples.
     
  3. sgbotsford

    sgbotsford Active Member

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    That makes sense: Normal growth requires that everything works.

    The reason that I asked this was the following notion:

    Swedish aspen is very susceptible to Bronze Leaf Disease. But in general, european aspen is not. All swedish columnar aspen are clones of a single sport discovered decades ago.



    Bronze Leaf disease doesn't affect all european aspen. There have been cases in trembling aspen too, but again, it doesn't affect the entire population, so there is a genetic component to susceptibility.

    It occurs to me that the following scenario may work:

    Locate several rural sites with no swedish aspen for a few miles, and ideally no native aspen either. Becuase the spores can be airborne you want sites that are outside of reasonable pollen drift. I have had infected trees growing some meters away from non-infected trees for several years at a time, so it takes unusual conditions to spread far.

    Locate a supply of seed run european aspens. Get a diverse set.

    Grow to a few feet high. Expose to BLD. Destroy any that show symptoms.

    Now you have a population of resistant trees that aren't columnar.

    Plant groves of seed run aspen and a small number of columnar aspen. Due to the risk of getting an infection this step should be replicated in several locations out of mutual contamination range. Cut down the male seed run trees as they make their sex known. You may want graft further known female twigs to the stump. (I have no idea how hard grafting poplar is.)

    Collect the seed from the female trees, and plant. This is an F1 hybrid, and so will most likely not show the columnar trait. (If it were dominant, it would be far more common.)

    Grow until a few feet high, but keep in pots so the roots don't interconnect.

    Expose to BLD. If they all croak, return to square run with different seed source.

    The survivors are now nominally carriers of the columnar gene, but it's masked by the normal growth pattern.

    Grow until they seed. Collect the seed, and start a new generation. If it's simple single gene recessive then 1/4 of the F2 off spring should be columnar. If it is a 2 gene mutation only 1/16 of them will be columnar.

    Test the columnar trees for susceptibility to BLD. If they all succumb then BLD susceptibility is on the same chromosome as the mutation for columnar growth. You're hooped. If they are not all susceptible, you now have established a population of columnar trees that can be used as further breeding stock for new columnar varieties.

    Would this work, or is my understanding of plant genetics naive?

    This does not take into account the possibility that columnar growth is polygenetic. As far as I know no one has attempted to work with swedish aspen to see how/if the trait is passed on.

    Columnar aspen don't seem to be at a severe disadvantage, so it's not clear to me why the gene would be selected against. Perhaps it has mutated only the one time.



     
  4. Daniel Mosquin

    Daniel Mosquin Renowned Contributor UBC Botanical Garden Forums Administrator Forums Moderator 10 Years

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    Maybe start from page 56 of this PDF: http://d-nb.info/1053846010/34

    Skimming through this, the paper is mostly about the mechanisms of columnar growth in apples, but it is possibly applicable to Populus.
     
  5. sgbotsford

    sgbotsford Active Member

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    Good lead.

    The apple mutation that takes up much of this paper is a branch sport, and is dominant. A columnar branch sport favours my notion (whim?) that fastigiate is a simple mutation, not a 47 genes have to conspire situation. Of course one example doesn't a law make.

    That said, this mutation clearly has wide spread influence. It's not just a skinny tree -- in effect the entire branch system has been subverted, with fruit spurs off the main trunk. I am a bit boggled that a single mutation can make such a drastic difference in form. Ah, homeobox genes....
     

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