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Permalink Reply by Banjo and Starbuck on November 2, 2008 at 12:48pm

Yes, a few generations back. She's starting to form a light widow's peak and her ears are getting pretty dark. The litter had two females with masks but the rest were red and white with blazes except for one total redhead. It was a big litter with a lot of variety.
Thanks for the great explanation.

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Permalink Reply by John Wolff on February 24, 2009 at 2:50am

PWCCA coat color genetics article
thanks for turning me onto this. I work in a genetics lab, and it's Monday night...I needed something to remind me how interesting my job is....
Science published a front-cover article on coat color in cats a few years back -- calico, tortoiseshell, that stuff -- it has a lot to do with patch size and X-chromosome inactivation (Lyonization), something we've been concerned with.
I want to learn about the white collar and face markings, why they're so hypervariable against the relatively stable black and red pattern (which I recognize in some German Shepherds, too). We have a gorgeous redheaded tri in our neighborhood without any of these white patches.

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Permalink Reply by Banjo and Starbuck on February 24, 2009 at 12:34pm

That's interesting. What application does Lyonization have in human genetics?
I first got into coat color genetics with my dwarf hamsters. One of them had a pretty unusual eye color mutation. Hamsters actually have a ton of variations. Here's a cool link with nice pics: http://www.hamperhams.co.uk/dwarf/hhpage1.htm
I'm just a starving artist, so I need to get my hard science fix where I can!

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Permalink Reply by John Wolff on February 24, 2009 at 1:20pm

To achieve dosage compensation, one X in females is turned off permanently and at random in every cell, else females would have a double dose of the X genes. Since it occurs at a very early stage in embryogenesis -- as few as a dozen cells(?), -- females can be a 50/50 mix of active paternal X & active maternal X, but it is possible for a female to be skewed towards one or the other, perhaps even having ONLY the maternal or paternal X active.

You can tell which X is active by assessing its methylation status (we think). There's an enzyme that runs around attaching methyl groups to the DNA at CCGG or CGCG sites (I forget), and this methylation seems correlated with X-inactivation. Some restriction enzymes are sensitive to this, so they won't cut methylated restriction sites. So it's easy to tell (in theory).

This is handy for telling whether a population of cells is clonal (one ancestor) or polyclonal. Handy in cancer research. Only works in females heterozygous for X-linked genes with methylation-sensitive restriction sites (we used the Human Androgen Receptor locus, HAR).

A postdoc in our lab used this to show why a girl was color-blind when her identical twin was not: they were both heterozygous for color blindness, but her X-inactivation pattern was completely skewed to the X with the colorblindness gene (it's X-linked recessive, usually showing up only in males). That's an epigenetic phenomenon. Monozygotic female twins can be different even though they're genetically identical.

I used it to show that Dupuytren's Contracture is not a clonal process -- and then dang if I didn't develop Dupuytren's myself!

If you read that article, it does address the sable trait hypothetically as one of 4 alleles at one locus:
ay dominant for red
redheaded tri recessive for tri
backheaded tri recessive to redheaded tri
ay- sable: dominant for red, but not entirely dominant, allowing some black pigment if the dog has a tri allele (hypothetical)

So now I know why Gwynnie's daddy was a blackheaded tri and why AL's daddy was a red.

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Permalink Reply by Banjo and Starbuck on February 24, 2009 at 1:26pm

Makes perfect sense. I'm also a twin, and the part about colorblindness was new to me. How fun!

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