Editing X-inactivation (section)

==History==
In 1959 [[Susumu Ohno]] showed that the two X chromosomes of mammals were different: one appeared similar to the [[autosomes]]; the other was condensed and heterochromatic.<ref>{{cite journal | vauthors = Ohno S, Kaplan WD, Kinosita R | title = Formation of the sex chromatin by a single X-chromosome in liver cells of Rattus norvegicus | journal = Experimental Cell Research | volume = 18 | issue = 2 | pages = 415–8 | date = October 1959 | pmid = 14428474 | doi = 10.1016/0014-4827(59)90031-X }}</ref> This finding suggested, independently to two groups of investigators, that one of the X chromosomes underwent inactivation.

In 1961, [[Mary F. Lyon|Mary Lyon]] proposed the random inactivation of one female X chromosome to explain the mottled phenotype of female mice [[heterozygous]] for coat color [[gene]]s.<ref name="Lyon 1961">{{cite journal | vauthors = Lyon MF | title = Gene action in the X-chromosome of the mouse (Mus musculus L.) | journal = Nature | volume = 190 | issue = 4773 | pages = 372–3 | date = April 1961 | pmid = 13764598 | doi = 10.1038/190372a0 | bibcode = 1961Natur.190..372L | s2cid = 4146768 }}</ref> The Lyon hypothesis also accounted for the findings that one copy of the X chromosome in female cells was highly condensed, and that mice with only one copy of the X chromosome developed as infertile females. This suggested<ref>{{cite journal | vauthors = Beutler E | title = Glucose-6-phosphate dehydrogenase deficiency: a historical perspective | journal = Blood | volume = 111 | issue = 1 | pages = 16–24 | date = January 2008 | pmid = 18156501 | doi = 10.1182/blood-2007-04-077412 | doi-access = free }}</ref> to [[Ernest Beutler]], studying heterozygous females for [[glucose-6-phosphate dehydrogenase]] (G6PD) deficiency, that there were two red cell populations of erythrocytes in such heterozygotes: deficient cells and normal cells,<ref>{{cite journal | vauthors = Beutler E, Yeh M, Fairbanks VF | title = The normal human female as a mosaic of X-chromosome activity: studies using the gene for C-6-PD-deficiency as a marker | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 48 | issue = 1 | pages = 9–16 | date = January 1962 | pmid = 13868717 | pmc = 285481 | doi = 10.1073/pnas.48.1.9 | bibcode = 1962PNAS...48....9B | doi-access = free }}</ref> depending on whether the inactivated X chromosome (in the nucleus of the red cell's precursor cell) contains the normal or defective G6PD allele.