High Throughput Small Molecule Screen for Reactivation of FMR1 in Fragile X Syndrome Human Neural Cells

Cells. 2021 Dec 27;11(1):69. doi: 10.3390/cells11010069.

Abstract

Fragile X syndrome (FXS) is the most common inherited cause of autism and intellectual disability. The majority of FXS cases are caused by transcriptional repression of the FMR1 gene due to epigenetic changes that are not recapitulated in current animal disease models. FXS patient induced pluripotent stem cell (iPSC)-derived gene edited reporter cell lines enable novel strategies to discover reactivators of FMR1 expression in human cells on a much larger scale than previously possible. Here, we describe the workflow using FXS iPSC-derived neural cell lines to conduct a massive, unbiased screen for small molecule activators of the FMR1 gene. The proof-of-principle methodology demonstrates the utility of human stem-cell-based methodology for the untargeted discovery of reactivators of the human FMR1 gene that can be applied to other diseases.

Keywords: FMR1; drug screen; fragile X syndrome; gene reactivation; human pluripotent stem cells; small molecule.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Drug Evaluation, Preclinical
  • Fragile X Mental Retardation Protein / metabolism*
  • Fragile X Syndrome / pathology*
  • Genetic Loci
  • High-Throughput Screening Assays*
  • Humans
  • Neural Stem Cells / drug effects
  • Neural Stem Cells / metabolism
  • Neurons / drug effects
  • Neurons / metabolism*
  • Reproducibility of Results
  • Small Molecule Libraries / pharmacology*

Substances

  • Small Molecule Libraries
  • Fragile X Mental Retardation Protein