Interesting Fings!! Questions to be addressed.

The Lethal Roan Question ....

Is it possible that Rn/Rn in the absence of other roaming genes remains lethal, but when combined with other roaming patterns it is not?
On a molecular level, is it possible that something in the "alternative roaming" genes is acting effectively as an 'antidote' for Rn/Rn lethality?
Or is it possible that the Rn zygosity testing is picking up on non-classic-roaning within the same genomic region as the classic Roan gene?
Has any work been done on mapping the various rabicano-type roaning genes been done?
Or on the sabino-type (other than SB1) genes?

We know it's possible (obviously!) to have rabicano-types which show no real evidence for classic Roan patterning, and to have classic roans which show no sign of also having rabicano-type patterning, so it should be safe to assume that the various roaning-encoding areas are not closely linked.

There is clearly a link between the sooty gene and the way in which particular plant compounds are utilised - but what is the exact nature of this link?
Sugar beet is rich in plant betalain pigments. (Sugar / tyrosine compounds.) Is that pigment being taken directly into the hair shaft in some way?
Has anyone microscopically or otherwise examined the hairs in sooty animals to clarify exactly what kind of dark pigment we are finding in chestnut (red-based, ee) animals which by definition lack the ability to produce eumelanin?
What is the exact mechanism which gives animals with the sooty gene the ability to handle those plant compounds differently?
Are sooty animals more or less tolerant of dietary sugars than non-sooty animals?
Is there any forward-progression possible from the last question which could aid research into sugar intolerance in other species?

.... and Ben d'Or Spots ....

Other Potentially Heat-Sensitives?

Could heat-sensitivity account for the distinctive pattern-types in the bodies of animals with the pangare gene? If it affected only areas within a small temperature-range, it could account for the fact that hotspots (muzzles, bellies etc.) and coldspots (lower legs) seem to fade out while other areas remain undiluted. And pangare dilution is usually much more noticeable in winter coat than in summer coat, An enzyme-related change could produce this.
Agouti: it's been said that it doesn't resemble point-patterning in Siamese cats - but has anyone actually experimented with how external skin-temperature might affect it? What could be observed in an animal with reduced circulation in one leg compared to the others? Does shoeing (which restricts circulation in the lower leg) increase the dark hairs either by concentration of pigment, or by number of hairs?? Does having a leg / legs permanently bandaged through a coat change (maybe as a result of injury) reduce the dark hairs either by concentration of pigment, or by number of hairs?
Appaloosa varnish roan?

Are they working in the exact same way at the exact same stage of embryonic / foetal development?
What's the reason for the patterning? (manes, tails, lower legs). Is this heat-regulated or hair-type regulated - or a bit of both?
Any chance their workings could be much more similar than supposed?
Silver maps to ECA6 - where does flaxen map to?

Interesting Fings!!! Here are some questions to be addressed by the LabRats
Subject:	Updates?
The Lethal Roan Question ....
There has long been a question as to whether homozygous inheritance of the Classic Roan (Rn) gene is lethal. Recently, horses from some breeds, which "breed true" for roan, have been tested for roan zygosity, and have apparently tested out as Rn/Rn. However, if we look at pictures available of these horses, they are also all showing rabicano-type roaning. So here are the questions: Is it possible that Rn/Rn in the absence of other roaming genes remains lethal, but when combined with other roaming patterns it is not? On a molecular level, is it possible that something in the "alternative roaming" genes is acting effectively as an 'antidote' for Rn/Rn lethality? Or is it possible that the Rn zygosity testing is picking up on non-classic-roaning within the same genomic region as the classic Roan gene? Has any work been done on mapping the various rabicano-type roaning genes been done? Or on the sabino-type (other than SB1) genes? We know it's possible (obviously!) to have rabicano-types which show no real evidence for classic Roan patterning, and to have classic roans which show no sign of also having rabicano-type patterning, so it should be safe to assume that the various roaning-encoding areas are not closely linked.
Sooty Questions
Well, sooty is an interesting one. It's known that diet can influence the expression of the sooty gene: if you deny an 'unfashionable' smutty palomino access to such highly pigmented feedstuffs as sugar beet, the smuttiness will reduce or even disappear completely. My own recent experiments in 'sootifying' coats by feeding reasonably large quantities of sugar beet to animals showing evidence of sooty have shown that it is possible to intensify the darkness of the coat. And it does turn 'standard chestnut' to 'liver chestnut' in chestnut animals showing signs of sooty. So the sooty gene (despite recent claims that it is not responsible for liver chestnut colouring), is certainly one mechanism (though not necessarily the only one) which produces liver chestnut colour. Here are some questions: There is clearly a link between the sooty gene and the way in which particular plant compounds are utilised - but what is the exact nature of this link? Sugar beet is rich in plant betalain pigments. (Sugar / tyrosine compounds.) Is that pigment being taken directly into the hair shaft in some way? Has anyone microscopically or otherwise examined the hairs in sooty animals to clarify exactly what kind of dark pigment we are finding in chestnut (red-based, ee) animals which by definition lack the ability to produce eumelanin? What is the exact mechanism which gives animals with the sooty gene the ability to handle those plant compounds differently? Are sooty animals more or less tolerant of dietary sugars than non-sooty animals? Is there any forward-progression possible from the last question which could aid research into sugar intolerance in other species?
.... and Ben d'Or Spots ....
I've long suspected that Ben d'Or Spots are a 'minimal expression' of the sooty gene. One of the animals I worked the sootifying experiment on was a mare with a standard red chestnut coat, a couple of small Ben d'Or spots, and a few dark hairs in the mane and tail. She sootified - turned distinctly darker. And the Ben d'Or spots all but disappeared with the darkening of the surrounding coat. Ben d'Or spots are seldom present in the foal coat. And they don't always turn out the same year-on-year. Is it possible that they are initially appearing at sites where the skin (and hair root) is cooler due to changes in circulation resulting from injury (even minor injury). Roan animals get 'corn spots' on scars. This springs to mind if one considers the mechanism for the distinctive colour-patterning in Siamese cats (darker where cooler, due to heat-induced changes in enzyme activity in the production of pigment). And sooty, in general, tends to 'strike' on the cooler areas of an animal (noticeably less sooty on warmer areas such as muzzle, flanks, underbelly, etc.) Could sooty be heat-sensitive as well as diet-sensitive? Sooty animals always seem to be more sooty in their summer coat - could this simply be a result of doing the winter-to-summer coat change in a much colder ambient temperature than the summer-to-winter change?
Other Potentially Heat-Sensitives?
Could heat-sensitivity account for the distinctive pattern-types in the bodies of animals with the pangare gene? If it affected only areas within a small temperature-range, it could account for the fact that hotspots (muzzles, bellies etc.) and coldspots (lower legs) seem to fade out while other areas remain undiluted. And pangare dilution is usually much more noticeable in winter coat than in summer coat, An enzyme-related change could produce this. Agouti: it's been said that it doesn't resemble point-patterning in Siamese cats - but has anyone actually experimented with how external skin-temperature might affect it? What could be observed in an animal with reduced circulation in one leg compared to the others? Does shoeing (which restricts circulation in the lower leg) increase the dark hairs either by concentration of pigment, or by number of hairs?? Does having a leg / legs permanently bandaged through a coat change (maybe as a result of injury) reduce the dark hairs either by concentration of pigment, or by number of hairs? Appaloosa varnish roan?
Flaxen and Silver
Flaxen seems to produce exactly the same patterning in red-based coats as silver does in black-based coats. And both seem to produce thicker coarse hairs (mane, tail, feathers) than in non-dilute animals within the same breeds. Are they working in the exact same way at the exact same stage of embryonic / foetal development? What's the reason for the patterning? (manes, tails, lower legs). Is this heat-regulated or hair-type regulated - or a bit of both? Any chance their workings could be much more similar than supposed? Silver maps to ECA6 - where does flaxen map to?
Stripe, spot and leopard.
What's the relationship? Suggestion: check the DNA of the re-bred quaggas (minimally-striped, bred from Burchell's zebra, at the Quagga Project) against 'standard' zebras to locate striping genes. Then check to see how they map on leopard-complex horses. Is there a link?
Fading black and mushroom.
Anecdotal evidence suggests these occur in related individuals. Mushroom ponies don't appear 'red' or 'leached red'. Is some kind of 'fading sooty' replacing both red and black pigment in these animals?