Re: [SpaceAgeRobin] HYB; Questions

The original work of Austin was combining protohorn types together to produce a horned variety. This wouldn't have been necessary with a dominant gene. Horned varieties popped up regularly in the seedling patch of Tom Craig. A lot of the early SA had distorted petals as well so the converse of SA would be well formed flowers. As these are selected for breeding, the selection would be to diminished SA genes and thus a reduction in frequence with breeders selecting from many seedlings and looking for best form. 

If there is a second gene it would likely be an enabler gene that permits SA formation. Of course this is the converse of the Normalizer gene. A dominant normalizer gene. would reduce the number of SA seedlings but not eliminate it from a cross unless it was present 4 times. 

Chuck Chapman

"Neil A Mogensen" <neilm@charter.net> wrote:

>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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