Supplementary Materials

The PDF file includes:

• Methods
• Fig. S1. RA treatment changes mEPSC and mIPSC amplitudes but not frequencies of neurons differentiated from ES cells.
• Fig. S2. Electrophysiological characterization of FMR1 cKO iN cells.
• Fig. S3. Removal of FMR1 expression results in impaired RA synaptic signaling and homeostatic synaptic plasticity in iN cells differentiated from FMR1 cKO ES line #1 F33 cocultured with mouse glia or mouse neurons.
• Fig. S4. Removal of FMR1 expression results in impaired RA synaptic signaling and homeostatic synaptic plasticity in iN cells differentiated from FMR1 cKO ES line #2 F17 cocultured with mouse glia or mouse neurons.
• Fig. S5. Electrophysiological characterization of iN cells differentiated from normal and FXS patient iPS cell lines.
• Fig. S6. Homeostatic synaptic plasticity induced by RA is impaired in iN cells derived from FXS patients, when cocultured with mouse glia or cortical neurons.
• Fig. S7. Effect of RA on synapse density and morphology.
• Fig. S8. Homeostatic synaptic plasticity induced by synaptic silencing is impaired in iN cells differentiated from FXS patient iPS cells, when cocultured with mouse cortical neurons.
• Fig. S9. Homeostatic synaptic plasticity induced by synaptic silencing occludes RA-induced synaptic changes in iN cells differentiated from normal patient iPS cells.
• Fig. S10. Model of the molecular mechanisms underlying disruption of RA-dependent homeostatic synaptic plasticity in FXS as analyzed in human neurons.
• Legend for table S1
• References (90–95)

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Other Supplementary Material for this manuscript includes the following:

• Table S1. Raw data (provided as separate Excel file).