Supplementary Figures S1-S17 from GABA regulates electrical activity and tumor initiation in melanoma

Combined supplementary figures and figure legends. Supplementary Fig. 1: Switching requires direct contact between nascent melanoma cells and keratinocytes in vivo. Supplementary Fig. 2: Switching requires direct contact between melanoma cells and keratinocytes in vitro. Supplementary Fig. 3: Switching does not involve cell fusion between keratinocytes and melanoma cells. Supplementary Fig. 4: Exosome-like vesicles are transferred from melanoma cells to keratinocytes. Supplementary Fig. 5: GABAergic signaling is active in skin and melanoma cells. Supplementary Fig. 6: Melanoma cells express GAD1 and produce GABA. Supplementary Fig. 7: Disruption of GABA signaling blocks melanoma/keratinocyte communication. Supplementary Fig. 8: Specialized cell-cell junction signatures are enriched in melanoma cells and keratinocytes. Supplementary Fig. 9: Melanoma vesicles are present near specialized GABAergic cell-cell junctions in co-cultures. Supplementary Fig. 10: gad activation correlates with higher tumor burden in melanoma. Supplementary Fig. 11: GABA producing enzymes are expressed in zebrafish melanoma cells. Supplementary Fig. 12: Disruption of GABA synthesis blocks tumor initiation in melanoma. Supplementary Fig. 13: GAD expression/GABA treatment is pro-tumorigenic in a non cellautonomous manner. Supplementary Fig. 14: Switched keratinocytes are pro-tumorigenic in melanoma. Supplementary Fig. 15: LIF expression in keratinocytes drives melanoma cell proliferation. Supplementary Fig. 16: Zebrafish melanoma scRNAseq identifies GABA and LIF associated components in the TME. Supplementary Fig. 17: MYCN drives LIF expression in keratinocytes.