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Combining the three recessive gene mutations; Motley and (Anery & Amel = Snow) combine to render this beautiful Snow compound mutation. Typically, they have many subtle colors found throughout the spectrum of the Snow compound mutation.

What to expect:
Both male and female hatchlings look alike (essentially white snakes with some tainted shade of what Motley markings).  

Go to History for more details about the DIFFUSED / BLOODRED base mutation of this compound morph.

This compound morph results from combining the color mutation, Amel with the pattern mutation Diffused and the new Red Factor mutation.  As with most morph compounds that include the Diffused mutation, the Fire mutation‘s color affect is generally more diffused than a typical Amel corn, but nothing compared to Cayenne Fire mutants that possess the additional Red Factor mutation. Except for some of the color and pattern variants of this mutation compound, Fires arguably have much less color contrast than typical Amels and generally redder coloration. Essentially, the difference between a Cayenne Fire and a Fire would be less yellow (therefore orange), rendering a red on red albino corn snake.  Expect dramatically reduced white margins, compared to most non-pattern Amel type mutants.

The snake pictured was posed on a U.S. one-dollar-bill for color reference. 

What to expect:
Many Fire hatchlings look like little more than some Amel Corns, but the head should have some form of Bloodred head pattern, and the belly will be devoid of classic Amel Corn snake white & off-white checkering.  The belly pattern can have colors – and even pattern – but not organized checkering.  From a short distance, adults appear to be completely red or red/orange, but upon closer examination, most have a faint blotch pattern, and some will have minute traces of white on the scales around the posterior-most dorsal markings.

The Buf corn snake was discovered by Jan Notte (corn snake breeder in Europe https://www.slangenbroed.nl/) in 2001.  It is the first corn snake gene mutation to be identified as being dominant to wild-type.  Buf corns are generally more yellow or gold than most wild-type corns and combining them with Amel (called ORANGE) they resemble Creamsicle mutants (Bufs are not hybrids).  Bufs are relatively new to the United States so expect to see many new morph compounds of this beautiful mutation in the near future.  

Several breeders (myself included) have performed breeding trials to verify that Terrazzos are not allelic to other gene mutations.  Results were somewhat mixed – probably because people have been breeding mutations into Key Corns for so many years – but the general consensus is that most Key Corns are not allelic to current mutations.  I’ve personally bred Key Corns to Diffused (aka: bloodreds) and all the babies were phenotypes for Diffused mutants.  Many more breeding trials are in order.  Partly because of the diversity between many of the different Key habitants (including some South Dade County, Florida, corns that satisfy the visual Key Corn standard.

INTERSPECIES  HYBRID !

Formerly considered an intergrade of what were formerly two corn snake subspecies (Elaphe guttatus guttatusX Elaphe guttatus emoryi), Creamsicles are the final product of crossing the Emory’s Rat (aka: Great Plains Rat Snake) snake with an Amel corn. Since the new taxonomic classification assigns distinct species status to both, (Pantherophis emoryi and Pantherophis guttatus), Creamsicles are now officially considered HYBRIDS. ANY progeny from Creamsicles or any corn snake that have any degree of Emory’s Rat Snake genetics, is considered a HYBRID.  The albinos are called Creamsicles and the non-albinos are called Root Beers.

Beyond the HYBRID product of AMEL corn and EMORY’S RAT SNAKE, Creamsicle Okeetees have distinctively saturated orange colors, separated by broad (and shocking) white blotch margins.  Some of the richest color and contrast demonstrated in a Corn Snake Type.

Go to History for more details about the DIFFUSED / BLOODRED base mutation of this compound morph.

In 1997, we acquired a Bloodred female from an unknown corn snake breeder that had a few lateral patches ofwhite.  We bred her to one or two males over the next six years, but never reproduced the white patches, nor did we hold back any of her sons to breed back to her.  In 2003, she was bred to a male Bloodred that has considerably more white on his sides, but no white was demonstrated in any of the F¹ progeny.  Upon breeding two pairs of the F¹ babies together, approximately 50% of the F²s demonstrated various degrees of white on their sides.  Also, when breeding one of the F¹males back to the SMR original female, 50% of those progeny also had various degrees of lateral white patches.  This demonstrated that the SMR P/S Bloodreds were not alleles of the original male Bloodred gene that had similar random lateral white patches. 

At this time – in my opinion – insufficient data has been gathered to determine that P/S Bloodreds owe their atypical white lateral and facial markings to a gene mutation.  It is remotely possible that polygenetic traits are responsible for the atypical patches of white on the face and sides, based on confusing phenotypes.  While evaluation of Mendelian Phenotype Proportions points to the likelihood of a gene mutation, that cannot be definitely proclaimed at this time.

It is sometimes difficult to determine the inheritance of a trait or mutation when expression of the atypical feature is highly variable – as is the case with SMR P/S Bloodreds.  In other words, are the Bloodred siblings of P/S Bloodreds that lack lateral patches of white not P/S Bloodreds OR are they P/S Bloodred mutants that are at the lowest end of the 0-to-10 scale for white expression?  When proving the mode of inheritance via evaluation of Mendelian Phenotype Proportions in a single brood of snakes, visual expression is crucial.  Hence, if the expression of white in this morph can be so extremely variable, when citing the ratio of visual mutants compared to visual non mutants, the very description of inheritance can be in question.  I therefore honestly don’t know if P/S Bloodreds owe their distinctive pied-sided white appearance to a recessive mutation OR polygenic trait modifications. Breeding trials are constantly being evaluated.  The snag in this determination is the fact that there are many siblings of the P/S Bloodreds that lack white, but have the remarkably red sides that are devoid of markings (a virtually distinct collateral trait of SMR P/S Bloodreds).  This particular trait is not foreign to the base mutation, Bloodred, but in P/S Bloodred phenotypes, expression of this shocking red trait is definitely exaggerated, compared to non P/S Bloodreds in the hobby.  Hence, the question again, “are these non P/S Bloodred siblings of those with white, P/S bloods that are exhibiting no white OR is there an associative phenotype that exaggerates the red sides, even if they don’t exhibit lateral white?”.  Some have suggested that the lack of color in places (i.e. white patches) is an extreme expression of the genetic elimination of melanin/markings.  That perhaps the genetic erradication of markings – when expressed in its’ extreme – may eliminate not only the melanin, but the other chromatophore as well?

Aside from the random lateral white feature that is obvious in most members of this morph – compared to standard Bloodreds – is the extreme diffusion – even if they don’t demonstrate any of the randomly distributed white patches on the sides.  On most – even in the absence of lateral white patches – there is an obvious line of demarcation between the dorsal and lateral pattern fields – just above the half-way point on the sides (dorso–laterally).  This stark break line between dorsal and lateral markings also begs questions about the lateral white being a mutation OR variable expression of polygenetics. 

Go to History for more details about the DIFFUSED / BLOODRED base mutation of this compound morph.

At this time, this author suspects that P/S Bloodreds owe their atypical white lateral and facial markings to polygenetic traits versus simple recessive mutation. It is sometimes difficult to determine the inheritance of a trait or mutation when expression of the atypical feature is highly variable.  In other words, are the Bloodred siblings of P/S Bloodreds not P/S Bloodreds OR are they P/S Bloodred mutants that are at the lowest end of the 0-to-10 scale for white expression?  When proving the mode of inheritance via evaluation of Mendelian Phenotype Proportions in a single brood of snakes, visual expression is crucial.  Hence, if the expression of white in this morph can be so extremely variable, when citing the ratio of visual mutants compared to visual non mutants, the very description of inheritance can be in doubt.  I therefore honestly don’t know if P/S Bloodreds owe their distinctive pied-sided white appearance to a recessive mutation OR polygenic trait modifications.

Aside from the random lateral white feature that is obvious in most members of this morph – compared to standard Bloodreds – is the extreme diffusion – even if they don’t demonstrate any of the randomly distributed white patches on the sides.  On most – even in the absence of lateral white patches – there is an obvious line of demarcation between the dorsal and lateral pattern fields – just above the half-way point on the sides (dorso–laterally).  This stark break line between dorsal and lateral markings also begs questions about the lateral white being a mutation OR variable expression of polygenetics.