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Re: T+ Creamino with a T- albino?
[Re: ]
#655344
10/12/08 07:48 PM
10/12/08 07:48 PM
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Leyna
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Leyna
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Halo, actually, true albinos are unrelated to the original cremino line, same goes for the leu lines and the the cremino lines and leu lines and the albino lines... You can actually use leus to breed out albino lines and vica verca.
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Re: T+ Creamino with a T- albino?
[Re: Judie]
#656936
10/15/08 02:50 PM
10/15/08 02:50 PM
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Joined: Feb 2000
Posts: 5,363 Ok
Sheila
Serious Glideritis
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Serious Glideritis
Joined: Feb 2000
Posts: 5,363
Ok
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I have bred a possible albino het 66% that I felt looked like his father and mother who had produced albino and cremino, with a 100% het for WFB. I have one WFB female and one normal colored female. I was told that the cremino het has a very light head, sivery body. I have never seen just a cremino het, only a double one so I don't know what colors these girls are. Albino hets, Cremino?, Leu? They really don't look too much like a Leu het just yet. They need some more fur. Now the reason I bring all this up is because if the male is a 100% (this is his first time to breed), wouldn't that be similar to putting an Albino het to a Leu? Stacie don't forget - we are not sure about the source of the breeder Dai Green, but this would have been the same pairing as alfred. He was an albino with a 100% het Leu mosaic.
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Re: T+ Creamino with a T- albino?
[Re: gliderboy4life]
#661388
10/24/08 12:26 AM
10/24/08 12:26 AM
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stix
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stix
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if you breed just 2 greys can you ever get any other colors?
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Re: T+ Creamino with a T- albino?
[Re: BeckiT]
#661431
10/24/08 03:47 AM
10/24/08 03:47 AM
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big ern!
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big ern!
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Leucism is different from albinism in that it is a defect that can be traced to the differentiation of the cells in early development. To simplify it, the cells that are responsible for body pigment are derived from the neural crest. They are mutated and do not produce pigment. However, the pigment cells of the eyes are not derived from the cells of the neural crest, so the eyes aren't subject to the same lack of pigment.
To get a better understanding of genetics, it would be a good idea to look into how genes actually manifest themselves as phenotypes. Sometimes oversimplifying genetics causes more confusion(at least it did for me in some cases). It helps to have a better grasp of the whole picture for certain smaller aspects to make sense. Obviously this is beyond the scope of a forum post, but if you care, there are plenty of good sources of info on the internet.
Genes code for proteins that are made up of many many individual amino acids that form a chain of length which is determined by the gene. The sequence of amino acids in an enzyme, much like the sequence of DNA is very important in determining the role that the protein/enzyme will play. Mutations can affect DNA in a ton of different ways. Some have a large effect, some have no effect and some have a mild effect.
In the case of albinism, there is a defect in the gene coding for an enzyme called Tyrosinase. Enzymes are made up of a chain of amino acids that are coded for by the DNA. Enzyme activity is directly related to the sequence of amino acids. The catalytic behavior of an enzyme is derived from molecular interactions between amino acids(which are part of a large chain) that create a specific folded conformation of the chain that is necessary for the enzyme to facilitate a reaction. The way an enzyme folds can directly affect its catalytic ability. Mutations in genes coding for enzymes can cause loss of function, impair function slightly and in some cases increase function.
T+/T- albinos experience a defect in a key enzyme that catalyzes te first step in the melanin production pathway. T+ still have some function in the enzyme hence a mild degree of coloration. T- have no tyrosinase function at all. Its the same gene, but a different mutation of the same gene. In some cases all it takes is a mutation in one base pair of the DNA to cause a loss of function mutation. It all depends on where the mutation lies in the coding sequence. If it lies in a part of the DNA code that calls for an amino acid component of the enzyme that plays a key role in the folding of that enzyme, or in a part of the code responsible for the catalytic region of the enzyme, it's gonna cause a big difference.
For example: the amino acid cysteine forms disulfide bridges with other cysteines that are key to enzyme folding. If you have a long string of correct code, but you have mutation in the DNA that inserts a thymine(DNA base) rather than an adenine(another DNA base), the DNA will code for the amino acid serine rather than the amino acid cysteine. The corresponding DNA codon(code sequence) for serine is 3'-ACT-5'(adenine, cytosine, thymine) and cysteine is 3'-ACA-5'(adenine, cytosine, adenine). All it takes is one properly placed mistake and the enzyme can be undone. Serine does not form disulfide bridges since it has no sulfur soooo ----> No disulfide bridge = no proper folding of the enzyme, and possibly no enzyme activity.
The more diluted creaminos may have more errors in the gene coding for tyrosinase causing a further decrease in the catalytic ability of the enzyme. This translates into less pigment produced than their predecessors. Hope this helps your head and doesn't hurt it.
Last edited by big ern!; 10/24/08 04:16 AM.
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