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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. 6. — A model of PRMT5 in regulating terminal differentiation of hypertrophic chondrocytes in the perinatal vertebral growth plate of the spine. (A) PRMT5 expressed in proliferative and prehypertrophic chondrocytes functions to regulate chondrocyte hypertrophic differentiation by controlling RUNX2 and IHH signaling. PRMT5 is required for maintaining postnatal expression of RUNX2, which is a key regulator of terminal differentiation of hypertrophic chondrocytes, and a positive regulator of MMP13 expression. PRMT5 also negatively regulates the expression of Ihh. (B) Prmt5 deletion in cartilaginous tissues of the spine leads to expanded Ihh expression in the perinatal growth plate and promotes the expression/accumulation of COLX. It also results in reduced RUNX2 and Mmp13 expression, which inhibits the terminal differentiation of the hypertrophic chondrocytes. These two processes synergistically lead to persistent hypertrophic growth plate and reduced bone formation in perinatal mouse vertebrae. AF, annulus fibrosus; EP, endplate; IVD, intervertebral disc; NP, nucleus pulposus; WT, wild type.