Re: RE:Hyb: Cytoplasmic inheritance was disease
It has been my experience that the abstract theoretical structure of the
universe (which includes what happens with irises) and the everyday encounters
with living plants and such do not necessarily have full equivalence. The
experienced reality and the conceptual structure more or less relate, but
there are always surprises--and forever there are revolutionary and
astonishing changes to the conceptual as new techniques for measuring,
looking, sensing develop.
If that didn't make sense--try this--Theory is one thing, every day life
Good theories do correlate with lived experience, but are always subject to
adjustment. The left-overs the "theories" (that's definitely not to be
understood as a negative term, by the way!) don't predict or explain--and
there are always a lot of them--are called "surds."
I like "surds." They make us work harder.
Here's one--the TB iris FRANK ADAMS has been observed to develop both
delphinidin and malvidin anthocyanins. The only other TB ever to be found
with malvidin in its flowers was a seedling from FRANK ADAMS and VIOLET
One would think that an iris with the parentage of (Ramese X Jerry) would
share what it contains with half the irises in the book. Not one has ever
been identified to have malvidin. I want to know why. I also want to
know--can Frank Adams be bred with something (it seems to refuse to be
selfed)--then the seedlings inbred until one of them emerges with the malvidin
<without> the always-present delphinidin expressed with it.
What color would it be? Is this perhaps another path to red in irises?
Or could it be that malvidin is the anthocyanin Don Spoon mentions in his
article about reds in the most recent *Bulletin* that isn't turned off by "I,"
the dominant white inhibitor?
These things don't fit the neat "theory" we work with about Iris color
genetics. They're surds. Good! Keeps life interesting, and makes the
seedling patch even more interesting.
Neil Mogensen z 7 western NC mountains
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