Fig. 6.

The ATOH1-POU4F3 synergy represents a conserved gene regulatory mechanism directing shared and divergent enhancer networks in different mechanosensory cell types. (A) Diagrams show the differential comparison of chromatin accessibility at the POU4F3-dependent ATOH1 targets specific to Merkel cells and hair cells. Of the 710 (Fig. 5D) POU4F3-dependent ATOH1 binding sites in Merkel cells, 523 were specific to Merkel cells compared to hair cells, while 187 were also accessible in hair cells. Of the 1,458 (Fig. 2C) POU4F3-dependent ATOH1 binding sites in hair cells, 683 were specific to hair cells, while 775 were also accessible in Merkel cells. Of the 187 + 775 common sites present in the two cell types, 833 were nonoverlapping (common). (B) Heatmap shows the chromatin accessibility and the binding profile of POU4F3 and ATOH1 at Merkel cell–specific, hair cell–specific, and common sites of POU4F3-dependent ATOH1 targets revealed in A. POU4F3 is able to weakly bind to Merkel cell–specific sites which are closed in hair cells and hair cell–specific sites which are closed in Merkel cells, consistent with its pioneer factor activity. (C) Motif enrichment analysis of POU4F3-dependent ATOH1 targets sites among Merkel cell–specific, Hair cell–specific, and common sites revealed in A. Different sets of transcription factor motifs are enriched in Merkel cell–specific and hair cell–specific POU4F3-dependent ATOH1 targets, suggesting a context-dependent specificity for the opening and activation of POU4F3-dependent ATOH1 targets in different cell types. (D) Genome browser representation of the μATACseq and C&R data at examples of the POU4F3-dependent ATOH1-targets that are Merkel cell specific (Slc1a2), common (Piezo2), and hair cell specific (Grxcr1).