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AB - THE Lyon hypothesis1,2 suggests that in the XX mouse and human female one X chromosome is genetically inactive after a certain stage in embryogenesis; that this 'inactive' X chromosome forms the Barr body, which can be identified at about the sixteenth day in the human embryo; that it is a random proposition which of the two X chromosomes in a given cell becomes the genetically inactive one; that once it is decided which X chromosome is to be the genetically inactive one in a given cell all descendants of this cell abide by the decision and have the same X chromosome inactive; and that the germ cell line does not participate in this process of X chromosome differentiation. The hypothesis suggests a mechanism: (1) of dosage compensation for the 'excess' genetic material in females; (2) of the observed phenotypic variability in females heterozygous for X-borne recessive mutations. The hypothesis requires the existence, in heterozygous females, of two populations of cells with regard to a particular trait for which the female is heterozygous. Beutler3 seems to have indirect evidence for such, in females heterozygous for glucose-6-phosphate dehydrogenase deficiency. All the genetic and cytological evidence supporting this attractive hypothesis1-4 will not be reviewed here. Some further evidence in its support will, however, be presented.

Lyon hypothesis-X-inactivation-mosaic formation - …

N2 - THE Lyon hypothesis1,2 suggests that in the XX mouse and human female one X chromosome is genetically inactive after a certain stage in embryogenesis; that this 'inactive' X chromosome forms the Barr body, which can be identified at about the sixteenth day in the human embryo; that it is a random proposition which of the two X chromosomes in a given cell becomes the genetically inactive one; that once it is decided which X chromosome is to be the genetically inactive one in a given cell all descendants of this cell abide by the decision and have the same X chromosome inactive; and that the germ cell line does not participate in this process of X chromosome differentiation. The hypothesis suggests a mechanism: (1) of dosage compensation for the 'excess' genetic material in females; (2) of the observed phenotypic variability in females heterozygous for X-borne recessive mutations. The hypothesis requires the existence, in heterozygous females, of two populations of cells with regard to a particular trait for which the female is heterozygous. Beutler3 seems to have indirect evidence for such, in females heterozygous for glucose-6-phosphate dehydrogenase deficiency. All the genetic and cytological evidence supporting this attractive hypothesis1-4 will not be reviewed here. Some further evidence in its support will, however, be presented.

Lyon hypothesis-X-inactivation-mosaic formation 1

Lyon hypothesis | Define Lyon hypothesis at …

In 1949, Canadian physician and medical researcher Murray Barr (1908–1995) noticed a dark body in the neurons of female cats. It was later identified as a structure found only in the nucleus of females. It was named a Barr body in honor of its discoverer. The Lyon hypothesis refers directly to a Barr body. It was proposed by English geneticist Mary Frances Lyon (1925–) in 1961 that a Barr body is actually an inactivated X chromosome. According to this hypothesis, female mammals sequester one X chromosome in each of their cells during the early stages of development. This folded chromosome becomes the dark body of Barr’s observation. This means that both males and females rely on the information from only a single X chromosome. Therefore, it is only one X chromosome that provides genetic information in both males and females.

THE Lyon hypothesis1,2 suggests that in the XX mouse and human female one X chromosome is genetically inactive after a certain stage in embryogenesis; that this 'inactive' X chromosome forms the Barr body, which can be identified at about the sixteenth day in the human embryo; that it is a random proposition which of the two X chromosomes in a given cell becomes the genetically inactive one; that once it is decided which X chromosome is to be the genetically inactive one in a given cell all descendants of this cell abide by the decision and have the same X chromosome inactive; and that the germ cell line does not participate in this process of X chromosome differentiation. The hypothesis suggests a mechanism: (1) of dosage compensation for the 'excess' genetic material in females; (2) of the observed phenotypic variability in females heterozygous for X-borne recessive mutations. The hypothesis requires the existence, in heterozygous females, of two populations of cells with regard to a particular trait for which the female is heterozygous. Beutler3 seems to have indirect evidence for such, in females heterozygous for glucose-6-phosphate dehydrogenase deficiency. All the genetic and cytological evidence supporting this attractive hypothesis1-4 will not be reviewed here. Some further evidence in its support will, however, be presented.

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