At 07:45 PM 2/1/99 -0500, Roening, Marcus (US Sales) wrote:

>The bird was was a bright off-white in color when seen with binoculars.
>However, with the help of a good scope, it was possible to see some very,
>very pale brown markings towards the back of the bird. These markings were
>somewhat more obvious when the bird flared it wings momentarily before
>diving. It also appeared there was some pale brown on the tail, but again
>it only showed when diving. On the front half of the bird, the only pale
>marking seen was on the neck where the black ring would normally be.
>
>The iris was black.
>
>The feet were pink and the bill was a pale yellow.
>
>So does this make it an incomplete albino loon? Or could the pale markings
>be some carotenoid pigments, versus very reduced melanin.

This is very interesting. I can't help with the Pettingill classifications,
which I find confusing, but I'll hazard some comments on mechanism.
Ignoring the iris for the moment, the off-white with pale brown in
locations where one would expect the darkest pigmentation sounds like a
very, very low activity of the melanin-forming enzyme (tyrosinase). The
pink feet and pale yellow bill can be explained as carotenoids, unaffected
by tyrosinase levels, as you suggest. The note about the neck ring is
interesting: I don't have a lot of experience with loons, but should the
bird be in winter plumage and missing the neck ring anyway? It would be odd
if the plumage cycles were disrupted as well as the melanin production.

The black iris confuses the picture. In mammals at least, the pigment in
the eye and not in other tissues would suggest a spotting/pied mutation
that affects the neural-crest-derived pigment cells but not the retinal
pigment cells. But I would expect a spotting mutation to give areas,
however large, of completely white tissue, not off-white with pale brown,
since the pigment cells should be absent from the affected areas. On the
other hand, in mammals I would expect a tyrosinase mutation to affect the
retinal pigment cells as well.

One possibility is that the tyrosinase gene has been duplicated in birds,
with one copy specialized for expression in retinal cells and the other for
expression in neural crest -derived cells. I have no idea whether this is
actually true, but it would not be an unusaul thing to happen in evolution.
Both eye structure and pigments are more complicated in birds than in
mammals. Another, perhaps more likely, scenario is that there are separate
genes or regulatory elements controlling the expression of tyrosinase gene
in eyes vs. other body parts, and the loon has a defect in the body color
controlling element. This would be a type of patterning mutation. There
might be enough genetics known in chickens to address the likelihood of
these explanations or others, but I'm not familiar with that literature.
Can any of our aviculturalists or ornithologists help out?




Paul Talbert
Fred Hutchinson Cancer Research Center
Seattle