RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders

Wojciechowska, Marzena; Olejniczak, Marta; Galka-Marciniak, Paulina; Jazurek, Magdalena; Krzyzosiak, Wlodzimierz J.

Similarly, in a few other transcripts with expanded repeats associated with human neurodegenerative diseases, we observe various representations of modifying factors that may potentially stimulate or inhibit RAN translation (Supplementary Figures S2a-w) regardless of whether the repeats are located in noncoding or coding portions of the diseases-causing genes. Structure prediction and sequence analysis reveal some extra stabilization of repeat hairpins by the flanking sequences but do not show substantial differences in the abundance of AUG-like codons in the analyzed transcripts when compared with transcripts proven to be RAN translated (Figure 1 and Supplementary Figure S2) . Interestingly, we have observed a general tendency for a higher abundance of AUG-like codons in the antisense transcripts than in their sense counterparts. These results suggest that other transcripts with expanded and structureforming repeats may also be subject to RAN translation.