Abstract:
:Trinucleotide repeat expansions involving CTG/CAG triplets are responsible for several neurodegenerative disorders, including myotonic dystrophy and Huntington's disease. Because expansions trigger the disease, contracting repeat length could be a possible approach to gene therapy for these disorders. Here, we show that a TALEN-induced double-strand break was very efficient at contracting expanded CTG repeats in yeast. We show that RAD51, POL32, and DNL4 are dispensable for double-strand break repair within CTG repeats, the only required genes being RAD50, SAE2, and RAD52. Resection was totally abolished in the absence of RAD50 on both sides of the break, whereas it was reduced in a sae2Δ mutant on the side of the break containing the longest repeat tract, suggesting that secondary structures at double-strand break ends must be removed by the Mre11-Rad50 complex and Sae2. Following the TALEN double-strand break, single-strand annealing occurred between both sides of the repeat tract, leading to repeat contraction.
journal_name
Cell Repjournal_title
Cell reportsauthors
Mosbach V,Poggi L,Viterbo D,Charpentier M,Richard GFdoi
10.1016/j.celrep.2018.01.083subject
Has Abstractpub_date
2018-02-20 00:00:00pages
2146-2159issue
8issn
2211-1247pii
S2211-1247(18)30147-5journal_volume
22pub_type
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