Re: [SpaceAgeRobin] HYB; Questions

Chuck, your comment,

"You forgot the third possibility. That is partial dominace. Under this
theory  the protohorns would be 2 sa genes and horns three and possibly
flounces four sa genes. As the genes have been around since like, forever,
they would be thouroghly distributed so many plants ( as with pbf) will
havesome genes and like PBF, was considered to be dominant until a closer
look was made of it.

"As the the Thornbird pedigree. Only the crosses producing SA plants were
used. Any crosses not producing SA plants were not used so data does not
suport dominance. I could build a similar chart with PBF.

"The ratios produced fit a partial dominance idea better then a complete
dominance theory, without invoking a second set of genes ie: Normalizer gene
or suppressor gene. The variation of  expression also fit this idea as with
PBF were the expression of feature depends on environment and climate. This
variation in expression is not seen in dominant gene or recessive gene
control."

--is taken seriously, and was in the background in forming the plan.  This
is why the records for generation one and generation two of the "No SA"
crosses is so important.  Hopefully accurate ratios and types will be
adequate to differentiate a possible "Normalize" from lack of the recessives
condition.

The reason I've taken the inital track (obviously flexible, I should add,
and subject to change should the data we acquire prove useful in ratios
counted) of an external "Normalizer" control, as such things can and do
exist ( dominant white is an example of the type, and appears to be a result
of a defect or blocker of the enzyme moving leucodelphinidin to delphinidin
where the pigment formation can continue.  That's a complex matter that
would be of interest discussed elsewhere).  The Sutton flounce on Wild Wings
is the kicker.  That cannot occur (or could it?) if a single Dominant to the
SA recessive was disbled--or an epistatic Normalizer was disabled.  The
reason I excluded (tentatively) the destruction of the dominant is that
among the thousands of seedlings Keppel and Ghio have raised from this type
of breeding with closely related sets of parents have never produced SA
varieties, at least any that were noted.  I believe Keith dislikes the SA
condition, but he's knowledgeable and honest and would not discount or
ignore the emergence of SA's within his lines.  He might not save or
introduce any, but he wouldn't blind himself to their presence.  They're not
there.

The first would fit your interpretation and may well be correct.  Two
generations of offspring from a few of the known non-producers hopefully
would differentiate.

Obviously the genetics of SA phenomena is more complex than a single gene
because of the tissue formation variability, including both beard spine and
fall tissues, and in a few extreme cases, even the inside base of the
standards, but the original Austin crosses, and those of two California
hybridizers, Tom Craig's BEARDED LADY, and another I cannot for the moment
pull up in memory do suggest the emergence of a hidden recessive.  The
ancestry of BEARDED LADY is from Sass plicata breeding, and is itself a
plicata form.

"Partial Dominance" certainly straddles the fence between the artificially
created categories of "Dominant" and "Recessive" which at first glance do
not seem to admit an intermediate status, but which SA phenomena do seem to
do, as do many other genetic controls.  As our knowledge of Molecular
Genetics grows so that not only is a specific factor identified, but its DNA
background both known and published the whole concept of the range from
"Dominant" to "Recessive" is likely to get a thorough overhaul.  I suspect
we will find ourselves looking at a continuum or spectrum of relationships
between fully "recessive" to "fully dominant."  The example touched on
above, "I" whites, is an example of a less than complete dominant as some
pigments come through in varying degrees (as in SILVERADO), and a remotely
possible condition where another is not blocked at all.

I say this, since if the recessive were present in diploid European Eupogons
for centuries, which does seem to be true, it seems unlikely it would not
have emerged fairly frequently, on the order of plicata, unless some other
genetic condition prevented its visibility in most cv's.  The emergence is
extremely rare, or at least rarely recorded in extant records.

I believe that lends weght to the idea of a "Normalizer" epistatic gene or
genes.  Other interpretations are not excluded thereby, however.

Neil Mogensen  z 7  Region 4  western NC mountains



 
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