Since the allele for colorblindness is located on the X chromosome, colorblindness?
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Is sex-linked. Sex linkage by definition involves all traits located on the sex chromosomes. Sex linkage doesn't mean that only males can be colour-blind, but it means that the sex of a child influences its chance to have that trait.\n\n(BTW "the" allele for colour blindness is crap... a normal human actually has 3 colour vision genes, two of these - "red" and "green" - on the X chromosome; meaning several types of colour blindness. A red or green can simply be left out when X chromosomes exchange DNA in egg cell formation, or you can have defective versions of either gene. As the third gene, that which codes for the blue receptor pigment, is located on another chromosome, there exists non-sex-linked colour blindness as well.)
463219
The trait is X-linked, there are two alleles, orange and black. In female mammals (including humans) one of the X chromosomes in each cell is shut off at a point early in embryonic development. Which X is turned off (the one with the orange allele or the one with the black allele) is random, but every cell that descends from that cell where it is turned off is the same. Some of these cells become skin cells that determine the color of the fur at that point. So, you can see where this is going, you get patches of fur that are one color and patches that are the other color randomly distributed over the cat's body. The male is either black or orange because it has only one X chromsome that never gets turned off.\n\nYou should be able to find more details on this and other cat genetics in a lot of places on the web.
164659
Red/green and blue color blindness appear to be located on at least two different gene locations. The majority of affected individuals are males. Females are carriers but are not normally affected. This indicates that the X chromosome is one of the locations for color blindness. Male offspring of females who carry the altered gene have a 50 percent chance of being color-blind. The rare female that has red/green color blindness, or rarer still, blue color blindness, indicates there is an involvement of another gene. As of 2004, the location of this gene was not yet identified.\n\nHe's right about the 7th chromosome,though.
675496
I don't see how it is false either. I mapped it out, and here's what I got. The eldest lady (grandma) could be XcXc (homozygous for colorblind). Grandpa must be XhY (hemizygous for hemophilia). This makes normal woman XcXh (the Xc would be normal for hemophilia and the Xh normal for color, masking the expression, resulting in normal). Husband must be XcY(hemizygous for colorblind). Son could inherit Xc from mom, thus being Xc (colorblind). Daughter could inherit Xh from mom and must inherit Xc from dad, thus being XcXh (the Xc would be normal for hemophilia and the Xh normal for color, masking the expression, resulting in normal). Please let me know if there is an error.\n\nSon cannot be normal; he'd be either Xc or Xh which is either colorblind or hemophilia.
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Color blindness is a result of a defect in the cone receptors in the retinas of the eyes. Color blindness is a male dominant trait, but is carried by the female. One male in twenty suffers from some form of color blindness, but only one in several hundred females are color blind.\n\nColor blindness is the general term used by most people but maybe in this politically correct world we should refer to it as chromatically challenged. However in reality the symptoms range from an inability to see one color, or shades of one color, to a lack of ability to see any color at all. Because it is a result of a cone defect, colorblind people are also prone to night blindness, and may have extreme difficulty in seeing in low light, or their color perception may be greatly reduced in low light.\n\nWhat color blind people actually see is hard to explain or describe to one who isn't colorblind, and probably equally hard to determine by someone else. To get an idea of the degree of difficulty, try closing your eyes and describing the color green to someone who cannot see or who is totally color blind.\n\nDescribe it without using descriptors such as it is the color of grass, etc. With the exception of blue (which has become synonymous with cold) and red (which has become synonymous with hot) it is very difficult if not impossible to describe a color except in terms of things which are that color, or in terms of another color.\n\nRegardless of the level of color blindness involved, almost all those afflicted can see dark objects on a light background. They may see them as shades of gray but they can distinguish. As the level of intensity approaches equilibrium the ability to distinguish diminishes.\n\nBy equilibrium I mean that the intensity of the colors involved approach each other (the dark objects become lighter and the background becomes darker).\n\nThe most common color perception problems are with certain color combinations such as yellow on green, green on red, red on green, blue on red, red on blue, and red on black. This last is particularly annoying and dangerous, because it means that unless we are concentrating, those flashing little LED displays become almost invisible. I have almost no perception of LED displays unless I am up close, and the diode is very bright.\n\nBy contrast since color blind people don't see color the same way others do, we tend to come up with combinations that are offensive to others but may be neutral or even pleasing or to us.\n\nSome color blind people tend to gravitate to bright, vivid colors because they can be detected more easily. Muted colors or low intensity colors (text, lines or bands where there isn't enough color to register) cause difficulty or are indistinguishable.
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x x -> color-blind female\nX Y -> normal male\n----\nx Y ; x X -> offsprings\n\ngiven the conditions, the chances are:\n0%  to have a color-blind daughter\n\n50% to have normal but carrier children\n50% to have color-blind children\n\n0% normal sons\n100% color-blind sons\n0% color-blind daughters\n100% normal but carrier daughters\n\nsince red-green color-blindness is a recessive trait, the mother would have the trait in both her x chromosomes. the father had normal vision so he would have the normal gene which is dominant for the trait. \n\nsince males get their x chromosome from their mother and the y chromosomes from their father, all sons borne would be color-blind because whatever the x chromosome they receive from their mother would have the gene for color-blindness. though the trait is recessive, this one gene would be enough to manifest itself because males only have one x chromosome. \n\nsince females get an x chromosome from each parent, all daughters would get a normal x chromosome from their father and an affected x chromosome from their mother. and because females have two x chromosomes and color-blindness is recessive, they would need to have two affected genes for the trait to be manifested thus all daughters borne would have normal vision. the dominant gene they received from their father would mask or overpower the affected gene they inherited from their mother. however, these daughters are also called carriers because the affected x chromosome they received from their mother can be passed on to their own sons wherein the color-blindness trait can then be manifested.
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From what I have read, it appears that it is autosomal dominant and is not X-linked as the gene most likely responsible lies on chromosome 1.\nHope this helps
30998
dyeing them if not that way than through family genes
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Complementation Testing\nOccasionally, multiple mutations of a single wild type phenotype are observed. The appropriate genetic question to ask is whether any of the mutations are in a single gene, or whether each mutations represents one of the several genes necessary for a phenotype to be expressed. The simplest test to distinguish between the two possibilities is the complementation test. The test is simple to perform --- two mutants are crossed, and the F1 is analyzed. If th e F1 expresses the wild type phenotype, we conclude each mutation is in one of two possible genes necessary for the wild type phenotype. When it is shown that shown genetically that two (or more) genes control a phenotype, the genes are said to form a complementation group. Alternatively, if the F1 does not express the wild type phenotype, but rather a mutant phenotype, we conclude that both mutations occur in the same gene.\nThese two results can be explained by considering the importance of genes to phenotypic function. If two separate genes are involved, each mutant will have a lesion in one gene while maintaining a wild type copy of the second gene. When the F1 is produc ed, it will expresses the mutant allele of gene A and the wild type allele of gene B (each contributed by one of the mutant parents). The F1 will also express the wild type allele for gene A and the mutant allele for gene B (contributed by the other muta nt parent). Because the F1 is expressing both of the necessary wild type alleles, the wild type phenotype is observed. \n\nConversely, if the mutations are in the same gene, each homolog will express a mutant version of the gene in the F1. Without a normal functioning gene product in the individual, a mutant phenotype occurs. \n\nEye color in Drosphila is a good model to demonstrate the complementation test. A wide array of spontaneous mutations have been studied. These experiments demonstrated that five genes (white, ruby, vermillion, garnet and carnation) controlling ey e color reside within 60 cM of each other on the X chromosome. The dominant wild type allele for each gene produces the deep red eyes. The mutant alleles produce a different color. If mutants from any of these five genes are crossed, the F1 would expre ss deep red eye color (wild type phenotype). \n\nFive different alleles (buff, coral, apricot, white and cherry) are also known to exist for the white gene, each representing a mutation at a different position in the gene. If mutant flies for any of the five white alleles are crossed, the F1 offspring would have a mutant eye color. Therefore, two genes involved in the expression of a phenotype complement each other. But complementation bet ween two alleles of the same gene does not occur
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see: http://en.wikipedia.org/wiki/Color_vision\nhttp://en.wikipedia.org/wiki/Color_blindness
12683
First off, the alleles that control hair and eye color are on more than one gene, so it isn't one specific gene, that control the color of hair or eyes. Brown hair is not a mutation. Allele wise you can either have light(blond) or dark hair, dark being dominant. As i stated it is a polygenic trait so varying gene configurations account for shades of hair.
58471
Chromosomes, either X or Y.
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Genetic predisposition.
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it is x linked recessive, meaning that a male will have the disease if his one x chromosome has the disorder.  for a female to actually have the disease, she has to have 2 defective x chromoxomes
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If there are two different alleles that cause different phenotypes, AND the phenotype of the het is indistinguishable from the phenotype of one of the homozygotes, then we say that that allele is completely dominant to the other, recessive allele.\n\nIncomplete dominance is usually used when the het has an intermediate phenotype due to haploinsufficiency, for instance, having one allele that codes for a working red pigment and one allele that codes for a broken pigment yields a pink flower that isn't making as much red pigment as the red homozygote.\n\nCo-dominance is when you can clearly see both gene products at the same time, like seeing blood cells with the A antigen and the B antigen.\n\n"Sickle-cell anemia illustrates that the terms dominance, incomplete dominance, and codominance are somewhat arbitrary. The type of dominance inferred depends on the phenotypic level at which the observations are being madeorganismal, cellular, or molecular. Indeed the same caution can be applied to many of the categories that scientists use to classify structures and processes; these categories are devised by humans for convenience of analysis."
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if this is a personal question, please talk to a doctor before having any children.\n\nthe math depends on if headaches are considered the same a migraines and if normal vision always means homozygous for non-blindness.\n\nbest case scenario is that half of the children are carriers for blindness but none are actually blind (like dad)\n\nIf mom is also a carrier, then (statistically)  half of their children would be carriers, one in four would be blind, and one in four would have normal vision.\n\nThe real statistics depend on a number of factors including what chromosome the gene lies, the number of genes that are involved in blindness, and a number of other factors (do they live in a lead house near a Chernobyl?)
147816
Probably very high in men, very very low in women because it is carried on the Y chromosome.  \n\nFor a woman to be colored blinded, she has to have an extra chromosome (XXY) which isnt very common.  \n\nNow this is what I remember from 5th grade science. I am no scientist or doctor.  lol