Just a little updated info
First, picture the LP gene as a "relay switch", which has two forms.
The normal version of this gene is the "off" position - we write it
as "lp". The mutation that Appaloosas have is the "on" version, and
we write it as "LP".
For a long time, it was assumed that dense white patterning, visible
at birth, and the LP gene itself were one and the same. In 2003,
when the genome scan was performed for LP and discovered its location
on equine chromosome 1, a very wonderful secondary finding came out,
one that helped to understand pattern inheritance in LP breeds.
Horses that were tested in the LP genome scan that had only
characteristics at birth, but were born with no coat pattern, still
came up "positive" for the mutation. This is an extremely important
finding. It means that while LP causes the traits of white sclera,
striped hooves and mottled skin, it doesn't, by itself, cause dense
white patterning. Something else must be present, another gene or
gene which works with LP, for this to appear.
Suddenly, a whole lot of phenotype data made sense, and horses like
those described here could have their progeny records explained.
You could even have a horse that had to LP carrying parents and assume that he
inherited a dominant copy from each, so his genotype was LPLP.
However, he didn't inherit any of the white pattern modifier genes we
now group together under the umbrella of PATN (for pattern). So, he
had a solid coat at birth, and later roaned a bit (LP is responsible
for that, it's actually the "fourth characteristic").
Being homozygous for LP, when bred to non-LP-carrying mares he passed
on a dominant copy to every foal he sired - had to! Some of those
mares had significant PATN genes to contribute to those offspring,
and voila - babies with blankets. If no significant PATN genes he received characteristics only..
Now for the E effect...this is the suppressing factor of the E gene or the black based horses..It was proven by another study that
Here are two of the most important things to consider when looking at
a minimally-marked LP carrying horse that can affect the expression
of what that horse has for PATN genes (white pattern modifiers):
1. Base coat colour of the horse
2. Presence or absence of white face and leg markings
With respect to the first, since black is the coat colour that causes
the greatest amount of suppression for white patterning (E-effect
study, Archer, unpublished) (Woolf 1990-96), it is quite possible for
a black horse to have one or more minor PATN genes, yet not express
them. It is unlikely that being black alone would cause total
suppression of a major PATN gene (like PATN-1, the gene we believe is
responsible for a full-body level of white patterning).
Consider black and all its derivatives the "deep end", bay and its
derivatives the middle zone and chestnut and its derivatives
the "shallow end". PATN genes are white stones of various sizes.
Put on the bottom of the pool in the shallow end, they are easy to
see. On the bottom of the deep end, only the biggest will be visible
from the surface.
Because of this potential for variable levels of expression, one
cannot speak in terms of absolutes. There may be a PATN gene present
that just doesn't show up on a given horse, but passed on to an
offspring that gives it all it needs to be maximized, it shows up on
that foal at a much higher level of expression.
Can a minimal have a hidden PATN like a non Characteristic ?
If a strong suppressing factor is present, a
horse might indeed be carrying one or more PATN genes that are not
being expressed anywhere near their normal level of expression.
