Fig. 5: Histological analyses of long bones from Col27a1 G682R KI mice.
a–j The growth plate of the developing femur of wild-type, heterozygous Col27a1G682R/+, and homozygous Col27a1G682R/G682R KI mice at post-natal day 1 stained with hematoxylin and eosin (A1–C1 and A2–C2 at higher magnification), safranin-O (D1–F1 and D2–F2 at higher magnification) and von Kossa (G1–J1 and G2–J2 at higher magnification). k–s The growth plate of the developing tibia of wild-type, heterozygous Col27a1G682R/+, and homozygous Col27a1G682R/G682R KI mice at post-natal day 1 stained with hematoxylin and eosin (K1–M1 and K2–M2 at higher magnification), safranin-O (N1–P1 and N2–P2 at higher magnification) and von Kossa (Q1–S1 and Q2–S2 at higher magnification). Homozygous Col27a1G682R/G682R KI mice displayed chondrodysplasia with reduced and disorganized proliferative zone and complete absence of columnar chondrocytes as compared with wild-type and heterozygous KI littermates (c, f, j, m, p, s). Although the length and overall structure of the growth plate is preserved in heterozygous KI mice as compared with wild-type littermates, some disorganization of the columnar chondrocytes can be observed (b, e, l, o) Histochemical comparison of Safranin-O and von-Kossa stains displayed no overt differences in proteoglycan accumulation and mineralization respectively between genotypes.
