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. 2021 Apr 14;11:8163. doi: 10.1038/s41598-021-87097-y

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed mechanism for the pathogenesis of FXTAS. (A) Expansion of CGG/CCG repeats in the 5′ UTR facilitates quadruplex (sense strand) and hairpin (antisense strand) formation. (B) Extended stability for the R-loop facilitates (C) quadruplex formation in FMR1 CGG mRNA due to the stalling of RNA polymerase. (D) RNA quadruplex-binding proteins facilitate RNA foci formation and (E) promote RAN translation to synthesize poly R or poly A or poly G aggregates. (B′–E′) RNA misprocessing and RAN translation associated with CCG antisense FMR1 mRNA. CCG repeats in RNA translate to either poly P or poly R or poly A aggregates. This figure was generated using Inkscape 0.91(https://inkscape.org/) software.