Ptip regulating SSC metabolism for safeguarding SSC quiescence and potency in maintaining skeletogenesis (IMAGE)
Caption
In the physiological condition of skeletogenesis (left), SSCs maintain a quiescent state for orderly differentiation which is regulated by the epigenetic signature. Especially at this state, glycolysis in SSC is suppressed by Ptip reducing the H3K27ac level at the Pgk1 gene promoter region. However, under Ptip-deficiency (right), SSCs exit the quiescent state and actively proliferate and differentiate, which is due to increased H3K27ac occupancy at the promoter region of Pgk1 gene leading to elevated glycolysis. Consequently, disordered cell arrangement occurs in the growth plate patterning of long bones, resulting in skeletal dysplasia. The glycolytic pathway can be pharmaceutically targeted to ameliorate SSC and skeletal disorders under Ptip deficiency. RZ, rest zone; PZ, proliferative zone; HZ, hypertrophic zone; Pgk1, phosphoglycerate kinase 1; 2-DG, 2-Deoxy-D-glucose; 2-MeOE2, 2-Methoxyoestradiol; Tss, transcription start site; H3K27ac, histone H3 lysine 27 acetylation.
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