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. 2019 Dec 17;12(12):dmm041251. doi: 10.1242/dmm.041251

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© 2019. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 3. — Loss of Prmt5 in osteochondral progenitors results in induced expression of COLX and depleted expression of PRG4 in the intervertebral disc. (A-D′) IHC analysis of type X collagen (COLX) (A,B) and proteoglycan 4 (PRG4) (C,D) in thoracic spine sections of Cre^– control (A,C) or Col2Cre;Prmt5^f/f mutant (B,D) mice at P10. The boxes outline the areas shown at higher magnification in A′-D′. Mutant mice demonstrated increased COLX signal in the endplate (B′, red arrowheads) and growth plate, and diminished PRG4 signal in the endplate and growth plate (D′), which was consistently observed in the Cre^– control mice (C′, red arrowheads) (n=3 mice for each group). Scale bars: 100 µm. AF, annulus fibrosus; EP, endplate; GP, growth plate; hGP, hypertrophic growth plate; NP, nucleus pulposus; pGP, proliferative growth plate.