Although GC differentiation proceeds gradually during gestation in marmosets (Mitchell et al., 2008), the present study shows that the pace of GC differentiation is much more rapid in the perinatal period than previously supposed.
Other ligands, WNT5A and WNT5B, appear to play opposite roles in determining the pace of chondrocyte differentiation [ 27].
In addition, PTHrP and IHH critically regulate the pace of hypertrophic differentiation in growth plate cartilage in a negative feedback loop.
First, IHH is required for synthesis of PTHrP and interacts with PTHrP in a negative feedback loop regulating the pace of hypertrophic differentiation [ 30, 31].
In this case Hedgehog signalling in the perichondrium activates the ubiquitin ligase subunit WSB-1 leading to degradation of D2 protein in the growth plate and increased PTHrP signalling, which regulates the pace of chondrocyte differentiation during early skeletogenesis [23].
Experimental evidence supports a model in which the specific distribution of Notch ligands endows distinct progenitor domains with the ability to influence the pace of cell differentiation in a domain- and cell-type-specific manner.
In this study, we hypothesize that activation or inhibition of NF- κB pathway can affect the pace of proliferation and differentiation in SCAPs.
IHh is produced by hypertrophic chondrocytes and, in turn, stimulates secretion of parathyroid hormone-related protein (PTHrP), which acts directly on the chondrocytes to slow the pace of hypertrophic chondrocyte differentiation during endochondral ossification [ 63].
Key among these are transforming growth factor-beta, IGF-1, fibroblast growth factors and PTHrP/Indian hedgehog, which together coordinate the pace of chondrocyte proliferation and differentiation.
This result indicates a rapid pace of evolution of recombination, within the time span of differentiation of modern humans.
