|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 9. Model linking skeletal size determination with digit separation in the
developing mouse limb. In this model [adapted from Mariani and Martin
(Mariani and Martin, 2003)],
N-Myc acts downstream of AER-derived FGFs in regulating the pool of
undifferentiated mesenchyme (green) in the early limb bud. The
undifferentiated mesenchyme gives rise to precartilaginous condensations that
are pre-specified to generate proximal [stylopod: forelimb humerous (blue)],
medial [zeugopod: forelimb radius and ulna (yellow)] and distal (autopod, red)
skeletal elements. After contributing to the growth of the limb segments,
residual undifferentiated cells are localized to the IDM, where they
contribute to the final stages of autopod patterning and are then eliminated
by programmed cell death. Their elimination terminates autopod patterning and
initiates digit separation. In the absence of N-Myc, the pool of
undifferentiated mesenchymal cells is reduced, leading to a proportional
decrease in all skeletal segments. The reduced pool of undifferentiated
mesenchymal cells is depleted during skeletal outgrowth, leading to loss of
the undifferentiated IDM that is targeted for cell death and required for
digit separation.
|
