Coat pattern identification confusion stems from a
misunderstanding of the term "roan" on the part of some registries.
The actual meaning of this term is quite simple - a mixture of
basecoat colour and white hairs. It doesn't mean spots of dark on
white, it means a mingling of white hairs with individual hairs that
are basecoat coloured.
Over time, the term "roan" has come to mean different things to
different people, and has been used as a sort of catch-all to label
such a wide variety of patterns, both Appaloosa-specific and other -
even greys get called roans!
When it comes to the Appaloosa roan and the Classic Roan
These are two types of roan patterning caused by two
different genes that each act their own unique ways. The LP(appaloosa)
gene, located on equine chromosome 1, is the main cause of the type of
roaning found in Appaloosas. Researchers believe that Classic roan
is caused by a gene called RN, and that it's a mutation of the KIT
gene, located on equine chromosome 3.
Classic roan comes in early (generally during
the first year of life, quite apparent after shedding of the foal
coat) and seems to be a bit more stable over time - comes in sooner,
and though it fluctuates a bit from year to year, and over the
calender year, it's fairly predictable and doesn't progress a whole
lot with age. At least one parent must carry a dominant copy of RN for the
foal to inherit it.. The classic roan has been the subject of several
studbook studies and is still thought to be homozygous lethal, meaning that there are no horses that are RNRN - Some breeders cross heterozygotes (RNrn), but
RNRN fetuses are not viable, and terminate naturally well before gestation is complete. However Ann T. Bowling of UC Davis was working on a study that refuted the homozygous roan lethal effect when she died in 2002. Her husband Michael was putting final touches on this study as of December 2004 and UCD was preparing to report the finding.. Previously thought was the apparent outcome in breeding roans to roans is roughly two
thirds roan to one third non roan.
What was thought was actually happening is that roan/roan is breeding two
heterozygous horses, and getting 25% nonroan, 50% heterozygous roan,
and seeing reduced fertility, since the 25% homozygous roan foals
never develop.
Also there are Sabino and Rabicano flecking which can mimic roan
if heavily expressed. Both of those also increase with age, as
opposed to classic roan, and are usually most prominent on the
barrel, and can be present on the face and legs, where as classic
roan does not effect the face and legs.
In contrast, LP-caused roan can do all sorts of odd things. There
usually isn't any present at birth, and often it doesn't start until
the onset of sexual maturity, or later, in some cases taking many
years to appear. It is generally progressive over time, and some
horses are affected so strongly they go from having almost no white
hairs to nearly white (BUT they retain their "varnish marks", the
areas where the number of darkly pigmented hairs is higher, on the
bony prominances of the face and body). Others get LP-caused
roaning, then lose some of it. Seems to happen with snowflakes,
a "clumped" form of LP-roaning that is very, very unstable in many
instances. At least one parent must carry a dominant
copy of LP and pass it on for LP-roaning to appear. Roaning
progresses over time, though not necessarily in a regular, gradual
manner. It may stop and start, and even go backwards in some
cases. Also, the distribution of white hairs is unique to LP-
carriers.
Also there are Sabino and Rabicano flecking which can mimic roan
if heavily expressed. Both of those also increase with age, as
opposed to classic roan, and are usually most prominent on the
barrel, and can be present on the face and legs, where as classic
roan does not effect the face and legs.
Clear as mud eh??
