Talk:Trinucleotide repeat disorders
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According to my genetics text-book (Thompson & Thomspons, Genetics in Medicine, 2007 pg 388): "...other disorders have now been found to result from the expansion of longer repeats; these include a tetranucleotide (CCTG) in myotonic dystrophy 2 (a close genocopy of myotonic dystrophy 1) and a pentanucleotide (ATTCT) in the spinocerebellar atrophy 10)." So it doesn't just have to be three base pairs. —Preceding unsigned comment added by 151.197.226.243 (talk) 01:03, 9 September 2007 (UTC)
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- Tetra and penta nucleotide repeat disorders would by definition not be trinucleotide repeat disorders. Friedreich's ataxia is an even longer repeat unit derived from an alu repeat I think.
Just a thought, this page could maybe do with some more clarification. Tri nucleotide repeat disorders are implied in the article to occur 'in the gene' coding for the disease related protein. More specifically, its in the promoter region of a gene where this tri-nucleotide repeat occurs. The sequence of the repeat itself isnt usually relevant, except for the fact it contains CpG sequences susceptible to methylation. Methylation of long repeated strands of these repeats causes silencing of the gene, and the associated disease.
—Preceding unsigned comment added by 87.194.219.186 (talk) 16:26, 19 October 2007 (UTC)
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- It isn't always in the promotor region, it's more often in the coding sequence, eg, polyGln disorders. It also doesn't often result in methylation of CpG islands. What you are describing sounds most like how fragile X syndrome works but that isn't a universal mechanism for triplet repeat disorders.
[edit] Non-viable di/tetra repeats
Explanation for increased viability of trinucleotide repeats compared to di/tetra repeats lies in that tri nucleotide repeats' extension and contraction does NOT cause FRAMESHIFT while other do. —Preceding unsigned comment added by 89.1.40.121 (talk) 00:54, 10 March 2008 (UTC)
