Trinucleotide repeat expansions cause several human genetic disorders. Repeat expansions in the non-coding regions of the genes often lead to down-regulation of gene expression. However, the underlying mechanism of the repeat expansion-induced down-regulation of gene expression remains is still unclear. We uncovered a repeat expansion-induced growth defect in Arabidopsis thaliana (Surehkumar et al, 2009), which shares striking parallels with the human disease Friedreich’s ataxia. In both conditions, GAA/TTC repeats expansion in the intron leads to down-regulation of gene expression caused by epigenetic silencing. Plants allow dissecting the developmental regulation of epigenetic silencing since within the same plants, some leaves (first to 6th) appear normal while others (Leaf 7th onwards) show the growth defect. This allows hypothesizing whether development regulates epigenetic silencing. We have previously shown that repeat expansions lead to small RNAs, which in turn cause gene silencing through the RNA-dependent DNA methylation (RdDM) pathway (Eimer et al, 2018), We have also uncovered that the SUMO protease called FOURTH ULP LIKE GENE CLASS 1 (FUG) is required for gene silencing pathway (Sureshkumar et al, 2023). Here we show that there is a developmental effect on the epigenetic silencing through a combination of phenotypic and gene expression studies. Our work has laid the groundwork to address the issue of cellular heterogeneity through single cell omics technologies. Our latest findings on the developmental regulation of gene silencing will be presented.