Figure 4.

Propionate signals through FFAR3-dependent and independent pathways in the nodose ganglion. (A) Graphical depiction of the experimental paradigm. Nodose ganglion explants were cultured from FFAR3 flox or vagal-FFAR3KO mice and stimulated with vehicle or 1 mM propionate for 12 hours; RNA was isolated and low-input sequencing was performed. (B) Venn diagram demonstrating the number of genes with expression significantly different between the treatment groups. (C) PANTHER pathway classification of genes that were altered in FFAR3 flox NG after propionate treatment but not vagal-FFAR3KO NG treated with propionate. (D–I) RNA sequencing results of genes within the “CCKR signaling pathway” (P06959) (D–G), leptin receptor (H), and early growth response 1 (I). (J) Prediction of altered transcription factors of “FFAR3-indendent” group (see Figure 3B) using the oPOSSUM database (Ho Sui et al., 2005). (K–L) NC vs. DIO top 50 genes (K) and altered PANTHER pathways (L). (M) Venn diagram showing overlapping “FFAR3-dependent” (see Figure 3B) and NC vs. DIO groups. (N–O) RNA sequencing results for C-X-C motif chemokine ligand 10 (N) and Inositol 1,4,5-Trisphosphate Receptor Type 1 (O). Error bars indicate mean ± SEM, n = 2–3 nodose ganglia pairs/treatment replicate, FDR-adjusted ∗p < 0.05.