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Harlequin Genetics, thus far
Topic Started: Jan 26 2014, 05:53 PM (2,346 Views)
HRoberts
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reh
Jun 7 2015, 12:52 PM
I am still convinced you cant see any differences in agouti gene in truebreeding eJeJ animals (no receptor, no way for agouti signal protein to work), so i would say a torted harli have to be eJe.

I cannot prove this but i read this on different ocassions on different places from harli breeders also.
I would agree with you, but have had a hard time test mating for just that. School has made it difficult to have this program on any kind of scale worth noting, if I was only working (instead of school + work + research + volunteering) I would have several more test mating animals that had nothing to do with the actual breeding program but were only there for the genetics aspect. Unfortunately choosing to research the color genetics while also trying to build up a breeding show herd is a challenge - we choose the best typed animals and those have been the crossbreds in our first few generations working with them. Finally starting to get a more homogenized group but still not close enough.

For now, keeping this dialogue open is sure teaching me a lot and I'm glad to have a group of people to weigh in when I have questions about what little I can observe! The plan is to finish the Master's in 14-16mo (eek!) and then on to PhD.

Interesting that you mentioned cysteine, I was thinking a methionine trial was in order to see about influence on clarity/number of bands. Again, something for after college. Thankfully my research interests are in poultry, not rabbits, so even if I get a job at a private facility I should be able to continue my rabbit hobby even if I had to give up the birds :/
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reh
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Quote:
 
The cinnamon tort harli seems like an ej version of the second rabbit you pictured

than its an AEej one ,not a tort

If melanoblasts differentiate early and then proliferate in cells making the same color its a matter of migration. lesser starting cells = bigger probability fore all cells in one band to have the same color (and maybe bigger probability for the cells to reach all skin areas - white toes)
Cystein is needed in melanosomes to form pigment, i dont know if it changes something during migration.
Do you know more about the trial, who wants to do it, ...? I am always interested to get in contact wit people investigating something in rabbits.
Edited by reh, Jun 9 2015, 11:51 AM.
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HRoberts
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reh
Jun 9 2015, 11:51 AM
Quote:
 
The cinnamon tort harli seems like an ej version of the second rabbit you pictured

than its an AEej one ,not a tort

If melanoblasts differentiate early and then proliferate in cells making the same color its a matter of migration. lesser starting cells = bigger probability fore all cells in one band to have the same color (and maybe bigger probability for the cells to reach all skin areas - white toes)
Cystein is needed in melanosomes to form pigment, i dont know if it changes something during migration.
Do you know more about the trial, who wants to do it, ...? I am always interested to get in contact wit people investigating something in rabbits.
I am thinking of doing the trial :) As far as I know there is little/no research ongoing with japanese genetics, I did find a somewhat recent paper (I think 2011, if I am remembering correctly) in the Netherlands.

Methionine withholding can slow down early embryo divisions, which is why I was thinking to look at Methionine first - as that could change migration. This is all a big "if" and will be several years before I could do the project within the scope I'd like to, but I will certainly be in touch with you if I get a chance to, or if I find others that are researching these genetics.
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reh
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I know of papers from Fontanesi, Italy only. Have you mismatched it or can you point me to the netherlands paper please?
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HRoberts
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http://www.biomedcentral.com/1471-2156/11/59
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reh
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Thats the one from Fontanesi (which says no expression of MC1R found in yellow parts of eJeJ).
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wildrabbits
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New update, the ej colorations of the chocolate tort harli is fading out considerably now he is AaEej for sure
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wildrabbits
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Neubunny has me wondering if anyone here has ever seen or worked with red and black harlequins due to high rufus mods? Also could high rufus in theory produce extra white magpie colors??
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HRoberts
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Not sure what you mean by "red and black" vs. orange and black (regular black japanese). We all try to get great color, but judges disagree on what that is. I like more of a dark NZ red type color (the good ones, not the faded out ones) but other breeders and some judges want more of a marigold hue.

We have not noticed any correlation between clarity of color and rufus, so no it would not affect magpies. Magpies are white or black (blue/choc/lilac), so there's no "extra white" to be had.
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wildrabbits
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I am still lost as to what exactly would cause 3/5 ej carriers to show harli markings while the other 2 show NO ej markings...

With my current understanding of things I want to say rabbits carrying 3 particular genotypes(Ccchd/eje, cchdcchd/eje or cchdc/eje)with rufus mods can cause a washed out effect/hidding ej markings at least during young age for 3 reasons.
1)From c and/or e causing the dark markings/spots to lighten to some extent
2)cchd+rufus causing a white effect where the red would be in the light spots caused by reason #1
3)cchd+wideband carrier pushing out some dark ej colorations on A_eje or at_eje genotypes but probably not with aa for as I understand it wideband doesn't have any phenotype difference with aa

Please share your opinions on these thoughts as well as your reasons for thinking why they could or couldn't work
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reh
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I have no idea how this should work in the known molecular biological ways how pigment is build. I tried to explain it several times. You can look in the posters i made for the europe show or search for and read the texts on Amys website.
Edited by reh, Jun 18 2015, 01:32 AM.
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HRoberts
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wildrabbits
Jun 14 2015, 10:17 AM
I am still lost as to what exactly would cause 3/5 ej carriers to show harli markings while the other 2 show NO ej markings...

With my current understanding of things I want to say rabbits carrying 3 particular genotypes(Ccchd/eje, cchdcchd/eje or cchdc/eje)with rufus mods can cause a washed out effect/hidding ej markings at least during young age for 3 reasons.
1)From c and/or e causing the dark markings/spots to lighten to some extent
2)cchd+rufus causing a white effect where the red would be in the light spots caused by reason #1
3)cchd+wideband carrier pushing out some dark ej colorations on A_eje or at_eje genotypes but probably not with aa for as I understand it wideband doesn't have any phenotype difference with aa

Please share your opinions on these thoughts as well as your reasons for thinking why they could or couldn't work
Are you positive all five are carriers? Did you test mate parents, and if so with what numbers and what crosses?

And no, I don't see c or e causing any lightening of dark spots. Also, rufus does not make more "red" area - it makes the area that was already "red" darker. We will call "red" orange from here on out as we're talking japanese gene genetics and that gives us orange and black (or fawn and blue, etc. etc.) so that we're keeping the lingo clear.

You can have ej_ animals with no markings with several combinations of other alleles on C, A, etc. These gene locations are a good starting point but I do not feel they are what is determining the amount of markings, in any way. The lightest marked animal I've ever kept for breeding is Aat CC ej_. Some of the best marked animals I've ever kept from breeding were Aat CC eje. The lightest marked magpie I've ever had was aa (chhl?cchl?) ejej. One of the best marked magpies I have had was A_ (cchl?cchl?) eje. I say cchl?cchl? because I see no difference in cchlc animals (magpies carrying REW) and cchlcchl, further evidence for no distinct interaction between the c series and the japanese gene other than changing orange/fawn to white, which also conveniently lines up with the molecular level genetics that fly over my head.

With only one litter from this crossing it would be extremely difficult to make any but the most basic of observations, and I think that with this gene that would be a grave mistake. If you're wanting to understand heredity of markings within your herd, breed another fifty or sixty kits from the same pairing or very closely related pairs and then see where you're at. This is why I started with the A series - it's one of the simplest to get ahold of each allele and follows a predictable pattern of dominance. We have dipped our feet into the pools of C, and of course are already in the E series with the primary interest (ej). It sounds like you have animals with too many unknowns to make any kind of conclusions.

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wildrabbits
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Edited by wildrabbits, Jun 23 2015, 10:32 PM.
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wildrabbits
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I don't know for sure what the flemish grandfather carried but both parents(of my newest Thur-Chin-Flemish hybrid babies) came from litters that each had only 1 REW so either parent could carry REW.

In this newest hybrid(Thur-Chin-Flemish) litter of 12(2 died early on) there were no REW's present so one or both of the parents doesn't carry "c". Also 6/12 would be considered "ej" carriers which is exactly how the standardized statics would be(these same statistics would also be true if "ej" is actually mutated self/dutch gene).

I should also note that the ee phenotypes also remained nearly exact to what the inheritable ee genotype would be(about 25%) if "ej" isn't actually an extension gene.

I have to say though HRoberts that your recommended test breeding method seems quite flawed for reliable phenotypes...
The only way to truly confirm the different genotypes to phenotypes would be by breeding non-related truebreeding genotypes f.e. aaejej to a completely unrelated aaee(with no "ej" in anywhere in its genetic background), then cross one of the resulting litter(all should be aaeje)to the same or another aaejej genotype. This would give you all the aaejej and aaeje phenotypes for proper study.

If however one or both of the ee phenotypes from my litter(which should be "eje") continues to not show markings and doesn't breed "ej" marked offspring than "ej" truly isn't an extension gene. THE HORRIBLE PART IS THAT I SOLD BOTH ee PHENOTYPE KITS BEFORE I FULLY REALIZED THIS!!! :wall: :bonk: :rant:

I do however have still have both parents and even have other undeniable Ee genotypes that I can cross with this same "Eej" mother as well as still being in contact with one of the ee phenotype buyers.
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wildrabbits
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Also another flaw I have to point out HRoberts is that cchlcchl and cchlc are VERY different colors! If you can't differentiate "seal" from "sable" with ejej that contradicts exactly what you said and would actually provide evidence that ej is heavily effected by C-series or vice versa.
Also "ej" must be heavily effected by the A-series f.e. atat, ata, and aa should NEVER make a chestnut color phenotype even with ej or ejej. Only A_C_D_E_(or Eej, Ee ext.) should come out as chestnut or chocolate chestnut(cinnamon).

http://www.thenaturetrail.com/rabbit-genetics/rabbit-color-genotypes-chart/

Its important to note that cchdc combinations are commonly known for making the whitest/least marked pearl/ermines which is why I suggested cchdc might be able to hide "eje"

I think looking further into the co-dominant/incomplete dominant interactions and the Harlequin breed origin might help some understand my huge hesitations and constant questioning with "ej"

I am not sure if this has been mentioned on this thread before but I have found multiple sources basically stating this same quote.
"The Harlequin Rabbit was developed in France in the 1800's from Dutch Rabbits with tortoiseshell colored fur. Two varieties were bred, one called the Japanese Rabbit, and the other called the Magpie Rabbit."

From this commonly spread history on the origin of harlequin rabbits it makes the most sense to me that ej is not an E-series gene but rather a mutation derived directly from self/dutch genes. My explanation would be "ej" acts as a switch that causes self colored/distorted dutch markings(self colors in place of the dutch white colors) when present and is not actually an E-series gene

The dutch gene and harlequin gene would be carried with the exact same statistics(and same statistics as explained for ej being an extension gene) among the offspring. This would explain both mysterious phenotypes of ej carriers(#1.randomized color effect on young "Eej" rabbits. #2.rabbits that should be "eje" but appear ee).

These two particular BRC/UKDRC description standards for dutch rabbits stated below hits home for me with my mystery adult Flemish Giant that I wondered if she could be Esej
"Flecking or Mealiness. Individual hairs more than one colour in self’s e.g. blacks should be black at the tip of the fur, that colour carrying down the fur as far as possible then merging into blue. In flecked or mealy exhibits the individual fur would be black, then dark grey then a deeper shade before merging into blue at the base"

"Chinchillation - A mixture of colours ticked with a darker shade, often found on the cheeks of yellows. The steel, pale and brown grey are chinchillated varieties to a certain extent"

Some of the earlier articles written about harlequin breeding that were mentioned on this page specifically speak markings/ticks/flaws that are heavily associated with dutch and mention specific effects when crossing harlequin with certain purebreds. Here is the link http://americanharlequinrabbitclub.weebly.com/history.html

I was trying to find another link I saw that basically showed early dutch/harlequin markings looking almost identical as well.
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