Re: Re: HYB: seedling survival comparisons

  I'm trying something new here.  I wrote a response to one post, then copied it and canceled, then pasted it into another post, so I can respond to two posts at once.
  An interesting thread here.

Linda Mann <lmann@volfirst.net> wrote:
  I can always make up some wild theories about nearly anything . My
gut says there might be. If there is a link, I'd assume it's
coincidental, not a necessity.
  ---This question of whether selection at the seedling stage is worthwhile has been asked by breeders for generations.  Breeders of all kinds of plants.
  Apple breeders commonly believe that large-leaved seedlings are better candidates for good apple varieties.  Studies in some crosses have shown this to be true.  But is it true only in certain crosses?  It is true in many crosses.
  In grad school, I was doing research on greenbug resistance in barley.  It was known that greenbugs couldn't live on one variety of barley, but could thrive on another, most.  I made a cross between a good adapted barley variety and a resistant one.  In thee F1, I just planted all the F1 seedlings in a tray with also a row of each parent variety.  When they were a couple of inches tall, I released greenbugs onto the tray, under a screen.  A week later, all the one parent seedlings were dead, and so were the greenbugs.  All the hybrids and all the resistant variety were alive and thriving.
  Backcrossing to the adapted parent variety, the first backcross seedlings about half were killed by greenbugs, the rest thrived and were happy as the greenbugs on them died.
  This is a common way to screen plants for insect and disease resistance.
  At the same time, Dr. Sorenson was breeding alfalfa.  He'd intercross his best plants in the greenhouse and get several cups of seed.  Then he'd germinate the seeds and turn a series of insects in on the seedlings, also spraying the seedlings with fungal spores from certain diseases.
  Finally he'd transplant survivers into a vat of sand and water, where the sand and water were never changed.  It was a foul-smelling putrid place.  Most of the remaining plants would die there of root rot.  Survivers were his parents for the next cycle.
  At first he was lucky to get one surviver through the first treatment.   He'd keep dong it with one set of parents until he got seveal, I forget the number per generation.  But after doing it enough generations, the survival rate would start to climb, and he'd add a step.  By the time I was there, he was using kinds of several insects and fungal spores.
  He was known for the health of his breeding populations.
  Clearly, selection for disease and insect can be effective at the seedling stage.
  But Dr. Sorenson had used thousand of seedlings per generation.  I don't see anyone here doing that.  So a proportional improvement in our smaller populations will not be very effective.
  And by not limiting our tests for survival to one pathogen at a time, natural selection will be still less effective.
   
  Linda Mann <lmann@volfirst.net> wrote:
What I've thought is that plants that thrive in the vale have the
physiology to cope with highly variable environmental conditions. They
can take both abrupt changes in temperature fall, winter and spring, and
alternating extreme drought and heavy constant rain in hot weather with
minor cell death. That implies they either have mechanisms to resist
damage or mechanisms to rapidly repair damage. I don't know whether or
not those same mechanisms would work the same way to resist or recover
from disease, but it seems they would, at least to resist disease.
  ---Studies in grain show high value in selection under adverse conditions.  But they generally had multiplication in alternate generations under excellent conditins so there would be lots of seeds to plant in the next generation in the adverse conditions again.
  Small populations are always a hinderence with genetics experiments.  Bummer.
  We do what we can.

From what I read about seed dormancy (all species, not just irises), the
chemical reactions that have to take place inside the seed and seed coat
can go either towards breaking dormancy or increasing dormancy. A seed
that doesn't easily come out of dormancy isn't going to germinate at the
first hint of warm weather in the middle of the winter. The mechanisms
are very different for disease resistance and difficult germination, but
I would expect them to both be present in cultivars that thrive here.

My theory about both types of survival here is that they are linked to
slowed response (i.e., slower growth, slower germination) to changing
environmental conditions. Has to do with carbon allocation (what the
plants do with photosynthate - use it to grow, for defense, or storage
for use in bad times).

Those are my theories. Is there a connection? Beats me 

between the difficulty of germination and the disease resistance of the
cultivar?
Betty W. in South-central KY Zone 6>
  ---Sounds like my former boss wondering if selecting for quicker germination would lead to shorter-lived perennial.  
  I told him, and I think that later research showed, that the seed dormancy was unrelated to health and long life.
  Some genes controle seed dormancy and then are turned off for teh rest of the plant's life.
  Some forms of disease resistance is based on chemistry inside the plant cell, and is going full blast as soon as the seed starts to germinate.  Other forms of resistance are based on thick skin with specialised chemicals in the skin, which will develope later. 
  For the former, infecting the seedling, or even germinating the seeds in filthy conditions, will indeed select for the genes controling single cell resistance.  If such genes are present.
  For the latter, selecition will be ineffective until the plant is well established.
  I suspect the latter is more important in iris.
  WAlter
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