Bicolor? - Page 11

Here is my pup's pedigree.

http://www.pedigreedatabase.com/german_shepherd_dog/pedigree/664185.html

I would post more updated pics but I always have trouble on this site.

It's gonna be OK Jen, its gonna be ok.....I think....

strange - my post didn't show up.  I said, jaggirl's pup appears to be black (IMO) as does her sire, and unless her sire is bicolor (which he does not appear to be) she would not be bicolor as black to black can only produce black - and this pup and her littermates pictured all appear to be black.

molly

There's two types of pigment (melanin).
Eumelanin - dark brown and black pigment
Pheomelanin - red and yellow (blonde) pigment

Gain-of-function Agouti alleles and loss-of-function Mc1r alleles each cause a pheomelanic phenotype, loss-of-function Agouti alleles and gain-of-function Mc1r alleles each cause a eumelanic phenotype, and animals carrying combinations of Agouti and Mc1r alleles with potentially opposite effects exhibit a coat color phenotype predicted by Mc1r rather than the Agouti genotype; in other words, Mc1r is epistatic to Agouti.

~Mammalian Genome, Volume 15, 798–808 (2004)

Daryl, your diagram is very good and illustates well the interaction between the two major genes controlling pigment balance, but, it's not really relevant here in this discussion for the reasons already given.

Are you suggestion that the interaction between these two genes accounts for the wide phenotypic expression between the palest saddle and the darkest bicolour?

If so, I'd be interested to hear, in your own words, how you think this is possible without allelic variation in these two loci.  Or are you suggesting there is allelic variation?

Have now done a quick search for reference to modifier genes that control pigment balance.  Haven't found much in scientific papers as, I presume, it's a given fact that they exist and there's no specific research so far to determine their location. 

Did find this bit though, by top researchers in the field - (my bold)

"In German Shepherd Dogs, the
nomenclature is especially complicated, since sable,
i.e., completely black hair, can be intermixed with
completely yellow hairs or with banded hairs. Various
authors have suggested ay, ag, aw, as, at, and a as
potential alleles (Little 1957; Willis 1976; Carver
1984), but in very few instances has it been possible
to distinguish allelic variation at Agouti from darkening
due to modifier genes distinct from Agouti and
Mc1r."

http://www.gdca.org/Fawnsable.pdf

Agouti and Mc1r genes at least, have been specifically studied in the gsd, and to say that they are not relevant in the expression of coat pattern is in my opinion, naive.  There are at least four that are positively connected with the coat-darkening colors in mice: the Agouti signaling protein (Agouti), attractin (Atrn), melanocortin-1 receptor (Mc1r), and mahogunin (Mgrn)

http://www.hhmi.org/research/investigators/barsh.html

Biology of Mammalian Pigmentation

Summary: Greg Barsh is interested in understanding the genetic and biochemical mechanisms responsible for mammalian color variation.

Our laboratory studies basic aspects of cell and organismal biology, as applied to mammalian development and disease. Most of our projects are based on the genetics of pigmentation, a model system that is experimentally tractable and relevant to human health.

Pigment Type-Switching
Agouti protein is a paracrine signaling molecule produced by specialized cells in the skin that causes melanocytes in the overlying hair follicle to switch from the synthesis of one pigment type, black/brown eumelanin, to an alternative form, red/yellow pheomelanin. Over the past several years, work from our laboratory and others demonstrated that Agouti protein promotes yellow pigment synthesis by binding to and signaling via a G protein–coupled receptor expressed on melanocytes known as the melanocortin 1 receptor (Mc1r).

Besides Agouti and Mc1r, mutations in at least 10 additional genes can interfere with the switching of pigment type. We recently determined that one member of this class encodes Attractin (Atrn), a large single-transmembrane protein that is expressed widely throughout the body but functions in melanocytes as an accessory receptor for Agouti protein. Expression of both Atrn and Mc1r on melanocytes is an absolute requirement for Agouti protein signaling; however, Mc1r lies genetically downstream of Atrn. Furthermore, in the absence of Agouti, mutations of Mc1r but not of Atrn can affect pigmentation. Thus, the intracellular effects of Agouti protein signaling are mediated via Mc1r, while cell surface interaction with Atrn permits signaling to take place. Our current effort is directed at understanding the biochemical basis for these observations and is likely to have wider implications for understanding how peptide hormones signal through G protein–coupled receptors.

Energy Homeostasis
An intriguing aspect of Agouti protein signaling is its ability to cause obesity and increased growth when expressed outside the skin. First recognized more than 100 years ago by gain-of-function mutations that cause obesity and a completely yellow coat, this phenomenon reflects the ability of Agouti protein to mimic a neuropeptide that we named Agouti-related protein (Agrp). Agrp is normally expressed in the hypothalamus, and signals via Mc3r and Mc4r to promote increased feeding and to reduce energy expenditure. Many aspects of the Agrp-Mc4r pathway are homologous or identical to the Agouti protein–Mc1r pathway. Furthermore, both pathways play important roles in human physiology, since loss-of-function mutations in Mc1r cause carrot red hair, fair skin, and freckling, whereas ~5 percent of humans with morbid obesity have loss-of-function mutations in Mc4r. Analysis of genetic variants in both hormones and receptors is helping us understand the structural determinants of receptor affinity and selectivity and also is providing a rational basis for efforts to develop small-molecule Mc3r and Mc4r ligands as pharmaceutical treatments for obesity.

Hypothalamic neurons that express Agrp are located in the arcuate nucleus, where peripheral signals of energy balan

http://www.chincare.com/Pages/PGdocs/mutationsgenetics.pdf

Among the most interesting group of coat color
mutations are those that cause regular patterns of
stripes or spots, as in zebras, tigers, leopards, or giraffes.
Although chemical or biochemical studies have
not been carried out, the components of such patterns
are likely to be eumelanin alternating with pheomelanin
(as in tigers or leopards), or eumelanin alternating
with no pigment (as in zebras).
Thus, the mechanisms operative in pigment typeswitching
± Agouti and Mc1r signaling ± may also be
responsible, in part, for regular pigmentation patterns.
However, in contrast to most coat color variants, an
ordered pattern of stripes or spots have not been identified
in laboratory mice or other rodents, which has
hampered molecular genetic insight into the underlying
mechanisms. Nonetheless, some limited conclusions
can be drawn from genetic studies in domestic
cats, where different alleles of a single gene, Tabby,
modify pigment type-switching in regular patterns
that may resemble tiger stripes or leopard spots.
Because a single Tabby genotype can produce patterns
that are either yellow alternating with black or white
alternating with black, the white areas probably represent
pigment type-switching rather than the absence
of pigment cells. Whether a similar phenomenon
explains alternating patterns of black and white in
ungulates, i.e., zebras, is less clear, however, since the
Tabby gene is clearly recognized only in the carnivora.
 

Characterization of the dog Agouti gene and a nonagouti mutation in German Shepherd Dogs

The interaction between two genes, Agouti and
Melanocortin-1 receptor (Mc1r), produces diverse
pigment patterns in mammals by regulating the
type, amount, and distribution pattern of the two
pigment types found in mammalian hair: eumelanin
(brown/black) and pheomelanin (yellow/red).....

Molly, in pictures yes they appear black. My pup's sire has a tan vent and tan toes. It is just not seen in the pics. He is registered as a black. The Czech Republic does not recognize bi color. Either they are black or black and tan. He obviously is not a black and tan. :)
My pup in her pic had the tan vent and tan toes at that age. Now the tan has gone up higher on her legs, around the front of the feet, and the insides of her rear legs. No other tan markings. If she was older, I would chalk it up to bleed through but the age she is, I am having her tested. Her tests may change what we know about blacks and bi colors.