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Polycomb repressive complex 2 regulates skeletal growth by suppressing Wnt and TGF-β signalling

Author

Listed:
  • Fatemeh Mirzamohammadi

    (Endocrine Unit, Massachusetts General Hospital, Harvard Medical School)

  • Garyfallia Papaioannou

    (Endocrine Unit, Massachusetts General Hospital, Harvard Medical School)

  • Jennifer B. Inloes

    (Endocrine Unit, Massachusetts General Hospital, Harvard Medical School)

  • Erinn B. Rankin

    (Center for Clinical Sciences Research, Stanford University)

  • Huafeng Xie

    (Children’s Hospital, Dana Farber Cancer Institute)

  • Ernestina Schipani

    (Medical School, University of Michigan)

  • Stuart H. Orkin

    (Children’s Hospital, Dana Farber Cancer Institute)

  • Tatsuya Kobayashi

    (Endocrine Unit, Massachusetts General Hospital, Harvard Medical School)

Abstract

Polycomb repressive complex 2 (PRC2) controls maintenance and lineage determination of stem cells by suppressing genes that regulate cellular differentiation and tissue development. However, the role of PRC2 in lineage-committed somatic cells is mostly unknown. Here we show that Eed deficiency in chondrocytes causes severe kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic differentiation and cell death with reduced Hif1a expression. Eed deficiency also causes induction of multiple signalling pathways in chondrocytes. Wnt signalling overactivation is responsible for the accelerated hypertrophic differentiation and kyphosis, whereas the overactivation of TGF-β signalling is responsible for the reduced proliferation and growth defect. Thus, our study demonstrates that PRC2 has an important regulatory role in lineage-committed tissue cells by suppressing overactivation of multiple signalling pathways.

Suggested Citation

  • Fatemeh Mirzamohammadi & Garyfallia Papaioannou & Jennifer B. Inloes & Erinn B. Rankin & Huafeng Xie & Ernestina Schipani & Stuart H. Orkin & Tatsuya Kobayashi, 2016. "Polycomb repressive complex 2 regulates skeletal growth by suppressing Wnt and TGF-β signalling," Nature Communications, Nature, vol. 7(1), pages 1-10, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12047
    DOI: 10.1038/ncomms12047
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