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Fig. 7. Regulation of bone development by MEF2. (A)
High-magnification frontal view of Hematoxylin and Eosin-stained sections of
mouse sternum. Left, wild-type trabeculated bone. MEF2C KO,
chondrocyte-specific deletion of a conditional Mef2c allele, which
results in a lack of bone owing to failure in chondrocyte hypertrophy.
MEF2-engrailed super-repressor, when expressed in the cartilage of transgenic
mice, also prevents ossification, whereas expression of a MEF2-VP16
super-activator results in the formation of excessive bone. (B) MEF2C
and MEF2D promote chondrocyte hypertrophy and vascularization of developing
bones by activating a network of transcription factors and signaling molecules
involved in bone development. HDAC4 imposes negative control over the network
by repressing the activity of MEF2 [adapted from Arnold et al.
(Arnold et al., 2007)]. IHH,
Indian hedgehog; PTHrP, parathyroid hormone-related peptide; RUNX2, runt
related transcription factor 2.
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