Of the three, the most faithful model of DS is the Ts65Dn mouse, which carries 132 genes that are syntenic with human chromosome 21.
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Since the late 1950s, scientists have also determined that a smaller number of DS cases (roughly 5%) are caused by chromosomal translocations.
(Because the translocations responsible for DS can be inherited, this form of the is sometimes referred to as familial DS.) In these cases, a segment of chromosome 21 is transferred to a second chromosome, usually chromosome 14 or 15.
Many early cytologists had, in fact, studied chromosomes from DS patients, but none had been able to detect a supernumerary copy of chromosome 21.
A breakthrough finally occurred in 1956, when Joe Hin Tjio and Albert Levan described a set of experimental conditions that allowed them to correctly identify the number of human chromosomes as 46.
When the translocation chromosome with the extra piece of chromosome 21 is inherited together with two normal copies of chromosome 21, DS results.
It is possible, however, for individuals to inherit a translocation of chromosome 21 without acquiring DS.
Thus, in his classic paper of 1866, Down noted that many children with mental retardation shared a common set of facial features, including an upward slant to the eye, a flat nose, and a large tongue.
He also noted that these children were born with their condition (i.e., the condition was ), and that affected patients had a shortened life expectancy.
The identification of particular translocation defects responsible for DS has been greatly facilitated by the of banding techniques that allow cytogeneticists to distinguish different breakpoints in chromosomes.