The A locus is the agouti locus or ASIP locus.  The A series is the agouti series, comprised of several possible allele types, not just in german shepherds, but in other breeds (i.e., dobermans) and species (i.e., mice, pigs).  Not all allele types (within the agouti series) are available in the genepools of each breed or species. One of which found in GSD's is a loss of function allele or null mutation known as "nonagouti black" or "recessive black"or "a", one of which isn't the ay allele which codes for a phenotype known as "fawn" or "golden sable" found in other breeds.

The aw type (as well as other types) can even be altered in phenotypical expression, due to epigenetic developments, cross affecting genes of another series and locus, or even due to affected regions within the allele itself, such as to cause dorsal or ventral loss of function.  "The ventral specific exons are located within a 3.1 kb region that is duplicated in the opposite orientation further upstream in the Aw allele [Lightner, 2009]"  For example, my rather lighter colored sable male has a black belly stripe.

"THERE IS NO, ZERO, ZILCH, NADA, NEVER IN A MILLION TRILLION BAZILLION CHANCES IN THE DEPTHS OF HELL that this sable puppy - if it's indeed a sable - came from that sire. NO CHANCE."  ~Molly

"This means that a sable cannot be produced without a sable parent (nor from black & tans or from bicolors, as some would argue)"  ~Daryl

Molecular analysis of reverse mutations from nonagouti (a) to black-and-tan (a(t)) and white-bellied agouti (Aw) reveals alternative forms of agouti transcripts.
http://genesdev.cshlp.org/content/8/4/481.full.pdf
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The agouti gene regulates the differential production of eumelanin (black or brown) and phaeomelanin (yellow) pigment granules by melanocytes in the hair follicles of mice. The original nonagouti (a) allele, which confers a predominantly black coat color, has been shown to revert to two other more dominant agouti alleles, black-and-tan (at) and white-bellied agouti (Aw), with an exceptionally high frequency. The at and Aw alleles confer phenotypes in which the pigmentation is not uniformly distributed over the dorsal and ventral surfaces of the animal; in both cases the ventral surface of the animal is markedly lighter than the dorsal surface due to an increase in phaeomelanin production. To understand the unusually high reversion rate of a to at or Aw, and to decipher the molecular events associated with the different pigmentation patterns associated with these three agouti alleles, we have characterized a, at and Aw at the molecular level.
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Black-and-tan is dominant to a but recessive to Aw. It is dominant to A across the ventral surface of the animal, consistent with yellow being dominant to agouti, but is recessive to A across the dorsal surface of the animal, which is compatible with the observation that agouti is dominant to black. White-bellied agouti, which confers an agouti dorsal surface and a cream color over the ventral surface, is dominant to the A, at, and a alleles. The a, at, and Aw alleles are also of interest because reverse mutations from a to at or Aw are more common than any other spontaneous agouti locus mutation (Dickie 1969).
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This implies that the original a mutation arose on a white-bellied agouti background. Furthermore, because form II transcripts are expressed in Aw but not in A, we propose that Aw is the true wild-type allele and that A actually represents a loss-of-function mutation in which form II transcripts are not expressed. This is of particular interest because both A and Aw have traditionally been referred to as wild-type agouti alleles. The proposal that Aw is the true wild-type agouti allele is not only compatible

with the molecular data presented here but is also consistent with reports that most populations of wild mice have a whitebellied agouti phenotype (Silvers 1979).