The long non-coding RNA FMR4 promotes proliferation of human neural precursor cells and epigenetic regulation of gene expression in trans.

摘要: Abstract Triplet repeat expansions in the Fragile X mental retardation 1 ( FMR1 ) gene cause either intellectual disability and autism, or adult-onset neurodegeneration, with poorly understood variability presentation. Previous studies have identified several long noncoding RNAs (lncRNAs) at locus, including FMR4 . Similarly to , is silenced by large-repeat that result enrichment of DNA histone methylation within shared promoter sequence, suggesting a possible role for this RNA pathophysiology X. We therefore assessed functional gain further insight into molecular processes X-associated disorders. work showed does not exhibit cis -regulation Here, we found chromatin-associated transcript and, using genome-wide chromatin immunoprecipitation experiments, alters state expression hundred genes trans Among regulated those involved neural development cellular proliferation. S-phase marker assays demonstrated may promote proliferation, rather than differentiation, human precursor cells (hNPCs). By establishing novel function hNPCs, lend support existing evidence epigenetic involvement lncRNA nervous system development, increase our understanding complex pathogenesis underlying neurological disorders associated expansions.