why is x inactivation an example of genomic imprinting?
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Two of the most prominent examples of allelic phenomena are X chromosome inactivation (XCI) and genomic imprinting. Because of XCI, only one copy of each X-linked gene is active in female cells (XX). Because male cells carry only one X chromosome (XY), they are inherently hemizygous for all X-linked genes.
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Sex chromosome researchers have long known that the vast majority of human and other mammalian females have two X chromosomes, while the vast majority of males have a single X and a Y, and only one X chromosome is active in females.
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Each person normally has one pair of sex chromosomes in each cell. Females have two X chromosomes, while males have one X and one Y chromosome. Early in embryonic development in females, one of the two X chromosomes is randomly and permanently inactivated in cells other than egg cells.
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Because of this, the presence of a CpG island is used to help in the prediction and annotation of genes. In mammalian genomes, CpG islands are typically 300-3,000 base pairs in length, and have been found in or near approximately 40% of promoters of mammalian genes. About 70% of human promoters have a high CpG content.
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A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons (no male-to-male transmission). X-linked recessive disorders are also caused by mutations in genes on the X chromosome.
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The recessive allele is expressed instead in the chromosomes to form an attached earlobe. It is not necessary that parents with attached earlobes should give birth only to the attached earlobe child.
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As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome (see dosage compensation).
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About half of individuals with Turner syndrome have monosomy X, which means each cell in the individual's body has only one copy of the X chromosome instead of the usual two sex chromosomes. Turner syndrome can also occur if one of the sex chromosomes is partially missing or rearranged rather than completely absent.
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Since males only have one X chromosome, any mutated gene on the X chromosome, dominant or recessive, will result in disease. Because females have two copies of X-linked genes, they will not be affected by inheriting of a single recessive mutation on an X-linked gene.
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Most cases of 47,XYY syndrome are not inherited. The chromosomal change usually occurs as a random event during the formation of sperm cells. An error in cell division called nondisjunction can result in sperm cells with an extra copy of the Y chromosome.
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This is because the X chromosome is large and contains many more genes than the smaller Y chromosome. In a sex-linked disease, it is usually males who are affected because they have a single copy of X chromosome that carries the mutation.
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In girls who have Turner syndrome, one copy of the X chromosome is missing, partially missing or altered. The genetic alterations of Turner syndrome may be one of the following: Monosomy. The complete absence of an X chromosome generally occurs because of an error in the father's sperm or in the mother's egg.
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As a result of the extra X chromosome, each cell has a total of 47 chromosomes (47,XXX) instead of the usual 46. An extra copy of the X chromosome is associated with tall stature, learning problems, and other features in some girls and women.
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It occurs as a random error during cell division early in fetal development. As a result, some of the body's cells have the usual one X chromosome and one Y chromosome (46,XY), and other cells have an extra copy of the X chromosome (47,XXY).
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It is a part of the XY sex-determination system and X0 sex-determination system. The X chromosome was named for its unique properties by early researchers, which resulted in the naming of its counterpart Y chromosome, for the next letter in the alphabet, following its subsequent discovery.
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An analysis of X-inactivation also argues against X-linkage as the cause of sex-bias [4]. Furthermore, LHON typically has an earlier age of onset in males than females. Present evidence therefore suggests that males are more susceptible to the mitochondrial defects.
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Families with an X-linked recessive disorder often have affected males, but rarely affected females, in each generation. For X-linked dominant diseases, however, a mutation in one copy of an X-linked gene will result in disease for both males and females.