Pie bald axolotls

[lou]

Do pie bald axolotls ( black and white like a cow) exist? Is there such a thing. If no, then why did they have to put a picture of one on the cover of the old axolotl book?

 

[Darkmaverick]

Hi Lulu,

Yes piebald and harlequin axies do exist. They are rare colouration and very hard to come by. There are some such photos from members from this site on the gallery.

Cheers.

 

[blueberlin]

I would add that the coloration is just an accidental grouping of pigments (like freckles) that happens to be pleasing to human observers and it cannot be inherited by offspring. And folks that actually find a larva with this color pattern most certainly do not offer to sell them. haha

-Eva

 

[John]

I would add that the coloration is just an accidental grouping of pigments (like freckles) that happens to be pleasing to human observers and it cannot be inherited by offspring. And folks that actually find a larva with this color pattern most certainly do not offer to sell them. haha

This is only true for some of the strange colour conditions but not all. The Harlequin axolotls in Scott's book are the type that breed true, but they seem to be very prone to disease, and so hard to come by.

 

[lou]

This is only true for some of the strange colour conditions but not all. The Harlequin axolotls in Scott's book are the type that breed true, but they seem to be very prone to disease, and so hard to come by.

very very hard to come by...

 

[big a little a]

This is only true for some of the strange colour conditions but not all. The Harlequin axolotls in Scott's book are the type that breed true, but they seem to be very prone to disease, and so hard to come by.

That's interesting - any idea why they are prone to disease? I mean, is it due to the line having been interbred to preserve that amazing look? Or is it due to genetic makeup or something? (I am not very scientific-minded, so a "gentle" explaination would be lovely ).

Zoe x

 

[Darkmaverick]

Hi Zoe,

If its of any similarity to genetics in other species, sometimes when certain external traits are selectively bred for (ie. harlequin), other undesirable traits are also selected for at the same time. The gene positioning (alleles) could be closely associated with the desirable trait, or the expression of the desirable traits will 'switch on or switch off' other genes that result in a myriad of conditions ranging from susceptibility to a malformation, poor conformation or weakened immunity.

Cheers.

 

[blueberlin]

The Harlequin axolotls in Scott's book are the type that breed true...

Interesting indeed - I've never heard of that before, but rather always that it is not inheritable. Neat stuff!

-Eva

 

[Strogg999]

As Rayson points out a mutation at any point of development in the pigment pathway can also carry a range of other effects, some of these have serious health implications.
In mammalian species “piebaldism” (white spotting) can be due to several types of mutated genes, all of which affect the migration of the pigment cells (known in mammals as melanocytes) from the neural crest. The neural crest is situated in the dorsal region of the growing embryo. These delays in migration can also affect other systems in the body because pigment cells are found not only on the coat but also in the inner ear, the brain, and the eye. Also, pigment cells aren't the only cells that migrate from the neural crest. Neural cells that enervate the intestines also undergo this migration. If the necessary neural cells don't reach the end of the intestine, the animal's intestines may not function properly, rendering the animal unable to pass faeces, which results in a condition known as megacolon.

There are many mutations that may affect the migration of cells from the neural crest. Each mutation is different in its effect and severity, each may be also modified by other genes. These types of spotting mutations may have a constellation of effects, not just on coat colour, but also behaviour, and sensory function. This is why white coat coloration, eye colour anomalies, deafness, and megacolon are often found together in these phenotypes. They are all the result of a delay in cell migration from the neural crest.
I did read a post on here recently where people have noticed a difference in behaviours and aggressiveness in wild type axolotls and mutations, this is also the case in most mammal species, and in particular piebald animals. As I mentioned earlier pigment cells also migrate to the brain, to areas such as the substantia nigra. This is a part of the midbrain that regulates mood, produces dopamine, and controls voluntary movement. They are also found in the locus ceruleus, which is part of the brain that deals with the stress response, and pigment cells also populate other areas such as the leptomeninges (membranes surrounding the brain), the dorsal root ganglia, and the cranial ganglia. The failure of pigment cells to reach these areas can have a wide variety of effects, such as a movement disorder (e.g. seizures), and diverse effects on behaviour and the individual's response to stress.
Pigment cells are therefore implicated in areas of the brain related to mood and the stress response. The connection between de-pigmentation and behaviour played a huge role in animal domestication. When early breeders selected for tameness, they were unknowingly selected for a different pigment cell migration in the developing nervous system, leading to calmer animals. A side effect of this selection for behaviour was the change in pigment cell migration in the skin, leading to a piebald coat. However, the flip side of this coin is that if depigmentation is extreme, the animal may have neurological impairments.


As for analogous genes in mammals which produce a harlequin phenotype, you have to remember that although the production of melanin pigments are virtually identical in both axolotl’s and mammals, the mammal has further modifications of melanin along the pigment pathway which enables them to produce the yellow/red pigments from melanin, where as the yellow pigments in the axolotl are produced differently. So although the harlequin coat colour variety in domestic species such as the rabbit may look very similar phenotypically to harlequin axolotls, the mechanisms in producing these yellow pigments are quite different.


Hope this helps the discussion,


Ed

 

[Darkmaverick]

Hi Ed,

That is a fantastic overview of how genetic traits can be interlinked in inheritance. However, for the same condition whether its coat colour, behavioural or even something we cannot visualise with our naked eye (chemokine, cytokine profiles etc), different species actually have completely different inheritance patterns. (Ie. blue eye white cats with deafness but not in dogs). This is one reason why genetics is so fascinating!

I am currently working on my dissertation in genomic studies in canine oncology (mast cell tumours and lymphoma) For people interested in veterinary genomics, or interested in how cancer is a 'genetic disease', here are some links for further reading.

http://omia.angis.org.au/

http://www.vetsci.usyd.edu.au/lida/

(Check out LIDA cats! I wrote two of the articles - Chylothorax and albinism )

Cheers.

 

[ianclick]

Totally off the topic please excuse me for this but it has always interested/puzzled me.

I have a brown eyed white pitbull whipett cross, parents both tan brindle with a white bib, the only white pup in the litter and totally deaf 9 pups in the litter. Now the proud mother of 6 black 6 week old pups all with good hearing father a tan brindle staffie.
I always assumed she was a mutant but was puzzled by her eye colour. Any clues?

 

[Strogg999]

I agree, fascinating indeed! Especially so the white spotting genes.

However, for the same condition whether its coat colour, behavioural or even something we cannot visualise with our naked eye (chemokine, cytokine profiles etc), different species actually have completely different inheritance patterns. (Ie. blue eye white cats with deafness but not in dogs). This is one reason why genetics is so fascinating!

This is quite relevant because it highlights how different genes on this pigmentation pathway can cause similar phenotypes and syndromes, but often it is a different gene that causes them.
With the blue-eyed white cats and deafness it is the dominant white gene (W) that is responsible. This particular gene mutation (of the c-kit gene) knocks out the kit protein, a tyrosine kinase transmembrane receptor, which is produced by the c-kit gene. The kit protein has a wide variety of functions and is involved in the development of blood stem cells (precursors to red and white blood cells), melanoblasts, and primordial germ cells, and melanoblast migration. So knocking out the kit protein will have a wide variety of effects! Another interesting point that you probably already know is that if the dominant white gene is activated at the wrong time in development, the result can be an uncontrolled proliferation of stem cells, i.e. cancer.

Ian,

In the dog, the Kit gene itself is implicated in the white coat colour patterning of some dog breeds. Here its genetical symbol is (s) and has several alleles. These range from the irish spotting allele s(i) e.g. Boston Terrier and Basenji. The piebald gene, eg, Cocker spaniels, Pointers, however the most extreme allele s(w) is found in Dalmatians, English Setters, white Bull Terriers, and white Boxers, where it produces a white coat, sometimes with pigmented spots. This allele is responsible for the high incidence of deafness in dalmations. It’s interesting to note here that dalmations that have coloured ear patches have a much lower incidence of deafness. This indicates that if pigment cells make it to the ear the hearing tends to be normal. A similar mutation in the Kit gene is also responsible for the coat colour pattern in Hereford cattle, but isn’t associated with deafness. However if you look at the breed you will notice they all have pigmented ears!

Ed

 

[Darkmaverick]

Hi Ed,

I am very impressed by your level of knowledge in veterinary genetics. A mutation in C-kit region has been identified to be the cause of canine Mast Cell Tumours. I am currently studying the variability/minute differences of the c-kit mutation in regards to prognosis and response to therapy of canine mast cell tumours.

My research also delves into investigating and identifying mutations in tumour suppressor gene and proto-oncogene regions in canine lymphoma. Hopefully, the research will shed some light on breed prevalence in Australian dogs where breeding strategies can make a difference in quality of life. Advances in veterinary medicine research can also cross over to human medicine, so i like to think i am helping to make a difference in some form.

I hope you don't mind me asking but surely you must do postgraduate level genetics (perhaps even veterinary genetics). There are very few people around who have the knowledge and detailed clarity in genetics especially across so many species. Are you a postgrad veterinarian or animal bioscientist? I think we can exchange some ideas.

Cheers

 

[Azhael]

Also completely out of topic...but i can´t help it xDD
I have a patch of totally white hair in my soul patch, and i have never been able to find a conclusive reason for it. I mean, i´ve read about piebaldism, about other partial albino conditions, but i haven´t found any that explains my single white patch of hair. Most partial albino conditions are linked to problems, or are supossed to have a different pattern...
So...sorry for hijacking the thread, but i´d apreciate some info on human "piebaldism".

 

[John]

Your hair is an example of recombination - basically the DNA for that patch of hair is not the same as the rest of you. This is not uncommon.

 

[Azhael]

Really..? just that?
I thought it was hereditary, since i have a cousin with a white patch on his head.
Wouldn´t a recombination occur if the tissue was damaged and had to be re-grown?
Genetics are not my strong point...the classes at college were booooring.

 

[Jake]

You could have vitiligo. http://www.patient.co.uk/showdoc/23069065/ The section "Who gets Vitiligo" might be useful.

That whole thing about the strange axolotls not breeding true might seem like the truth to all of you, and I completely understand your reasoning. However, I'd like to disagree. I have a white albino male that has fathered 8 "chimera" axolotls. There are 3 females that produced these 8 chimeras. Now tell me, if it's not genetic, how in the world did I end up with 8 (6 of them from one clutch)!? Most of these chimeras became very weak over time and died, but one (Pirate) has been doing well, and is a mother herself. In fact, I set up Pirate with the albino male/her father and one of her offspring was half leucistic half wild-type. I think people could raise a LOT more oddball axolotls if they'd raise more than a couple dozen larvae at a time. Pirate was one in about 200!

 

[Strogg999]

Azhael,

If the trait is being passed on through the generations it would indicate the human form of piebaldism, which is a mild analogue of the gene I was discussing earlier. Piebald humans tend to have a white forelock, no pigment of the forehead, and various patches of de-pigmentation over their bodies
It really is a well documented and antiquated mutation and you can find it mentioned and described in early Greek, Egyptian and Roman literature. It is a known as mark of distinction that has even been encompassed in people’s surnames, and families known for this mark carry such surnames as Whitlock, Horlick, Blaylock, etc.
For a good example of this gene in action in other species have a look at the hooded locus in rats. Here there are several hooded alleles which all cause different degrees of delay in the pigment cell migration process, and all of which cause various degrees of de-pigmentation in the coat. Other genes(modifying genes) then influence the layout of white markings. Homozygous Hooded rats (hh) have a pigmented head and dorsal stripe on a white body.


Rayson,

No nothing so glamorous as that :happy:, I'm just an amateur enthusiast of pigment biology. Although I am currently writing a paper due to be published on a newly discovered mutated gene in gerbils which has led to the discovery and re-identification of a new locus in this particular animal. Robinson and Leiper ([FONT=book antiqua, Times New Roman, Times]Leiper, B.D. & Robinson, R. 1985. Gray mutant in the Mongolian gerbil. The Journal of Heredity, 76, 473.) [/FONT] previously allocated the symbol of the locus as the G or greying locus but this has proved not to be the case.

I've kept a very wide range of small mammal species, but my main interest lies in their genetics and coat colour mutations :happy:

I have a gerbil website too lol, which has an extensive genetics section. There's even an old article on there about understanding piebaldism, which goes into a fair bit of detail on the subject in several species.

http://www.egerbil.com/genes.html

(hope i'm ok linking, but the info on the genes can be applied to many species)

Ed

P.S. I would love to read some of your current research. I have wrote a simple guide to neoplasia in gerbils that you can read on the website, and info on the subject is of great interest to me.

 

[Azhael]

Thanks Strogg...i´ve read about human piebaldism and i´m not sure it´s what i have. Although human piebaldism usually affects large areas of the face and sometimes the body, it can also be mild and localized..as is the case of the classic forelock(that as you mentioned sometimes is present throughout a bloodline). Mine though is in the soul patch, and nowhere else.
There are lots of cases of white forelocks, even localized white patches in eyebrows or eyelashes...It seems to always affect the forehead although in different degrees....but never the soul patch(I never found a report of a case with one single localized patch in the soul patch, but there are dozens of reports of forelocks, patches in the back of the neck, etc...).

Sorry if i´m obssesive xD I´m really curious about this.

 

[Strogg999]

It's interesting. How far have you researched it in your own family, you mentioned the cousin with the white patch too but on the head, are there any other examples further in family history? Often though, like I mentioned above, the de-pigmentation areas are greatly influenced by modifying genes. It could be you have a specific set of modifiers that allow the mutation only to be expressed or confined to the soul patch. At this level of expression though, when it's restricted to just the forelock or head region, it's very benign in nature.

Ed