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. 2023 Jan 19;19(1):e1010595. doi: 10.1371/journal.pgen.1010595

Fig 2. Hepatic Rps6-deficiency inhibits bile duct development.

Fig 2

(A) Photomicrographs of SOX9 IHC of WT (a, c, e, g, i) and ΔS6 (b, d, f, h, j) livers from E17 to P15 (Original magnifications, all x 125; 50μ scale bars) (AEC chromogen (red/orange), no counterstain). Note the gradual disappearance of SOX9-positive cells from the ductal plate in ΔS6 livers between E17-P3 and the abnormal position and expansion of SOX9-positive cells throughout the parenchyma from P7 onwards. (B) Photomicrographs of pan-CK IHC of WT (a, c, e) and ΔS6 (b, d, f) livers from P1 to P7 showing that the number of pan-CK-positive biliary cells in ΔS6 livers is also reduced at P1 and P3 (b and d) while their expansion at P7 (f) mirrors the increase in the number of SOX9-positive cells (A (h)) signifying emergence of a nascent ductular reaction. (Original magnifications, all x 250; 50μ scale bars) (AEC chromagen (red/orange), no counterstain). (C) Graph depicting quantitative analysis of the number of SOX9-positive cells around portal veins (PVs) in WT and ΔS6 livers at E17 and P1. ΔS6 livers have 20–25% of the normal number of SOX9-positive cells (mean values 7.8 vs 30.7 at E17; P < .0001 and 9.8 vs 47.5 at P1; P < .0001); 2-tailed unpaired Student’s t-test. (D) Graph showing average number of bile ducts per portal vein (PV) (bds/PV) in WT and ΔS6 livers at P1, P3, P7 and P15. While WT livers have an average of 1–2 fully formed bds/PV, ΔS6 livers have an average of < 0.5. Data are mean ± SEM; **** P < .0001; 2-tailed unpaired Student’s t-test.