Antero-posterior skeletal patterning is not dependent on continuity of the apical ectodermal ridge in the chick wing bud

1993 ◽  
Vol 188 (4) ◽  
Author(s):  
J.J. McCullagh ◽  
D.J. Wilson
Development ◽  
1984 ◽  
Vol 80 (1) ◽  
pp. 105-125
Author(s):  
Madeleine Gumpel-Pinot ◽  
D. A. Ede ◽  
O. P. Flint

Fragments of quail wing bud containing myogenic cells of somitic origin and fragments of quail sphlanchopleural tissue were introduced into the interior of the wing bud of fowl embryo hosts. No movement of graft into host tissue occurred in the control, but myogenic cells from the quail wing bud fragments underwent long migrations in an apical direction to become incorporated in the developing musculature of the host. When the apical ectodermal ridge (AER), together with some subridge mesenchyme, was removed at the time of grafting, no such cell migration occurred. The capacity of grafted myogenic cells to migrate in the presence of AER persists to H.H. stage 25, when myogenesis has begun, but premyogenic cells in the somites, which normally migrate out into the early limb bud, do not migrate when somite fragments are grafted into the wing bud. Coelomic grafts of apical and proximal wing fragments showed that apical sections of quail wing buds become invaded by myogenic cells of the host, but grafts from proximal wing bud regions do not.


Development ◽  
1977 ◽  
Vol 40 (1) ◽  
pp. 1-21
Author(s):  
Dennis Summerbell

Removal of the apical ectodermal ridge causes a reduction in the rate of outgrowth of the wing-bud and the loss of distal parts. More specifically it causes a short-term increase in cell density and cell death and a decrease in the rate of cell proliferation. The evidence supports the hypothesis of density-dependent control of cell division and suggests that there may also be a mechanism regulating skeletal length at the time of differentiation. An informal model is presented to explain the observations.


Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1385-1394 ◽  
Author(s):  
J.A. Helms ◽  
C.H. Kim ◽  
G. Eichele ◽  
C. Thaller

In the chick limb bud, the zone of polarizing activity controls limb patterning along the anteroposterior and proximodistal axes. Since retinoic acid can induce ectopic polarizing activity, we examined whether this molecule plays a role in the establishment of the endogenous zone of polarizing activity. Grafts of wing bud mesenchyme treated with physiologic doses of retinoic acid had weak polarizing activity but inclusion of a retinoic acid-exposed apical ectodermal ridge or of prospective wing bud ectoderm evoked strong polarizing activity. Likewise, polarizing activity of prospective wing mesenchyme was markedly enhanced by co-grafting either a retinoic acid-exposed apical ectodermal ridge or ectoderm from the wing region. This equivalence of ectoderm-mesenchyme interactions required for the establishment of polarizing activity in retinoic acid-treated wing buds and in prospective wing tissue, suggests a role of retinoic acid in the establishment of the zone of polarizing activity. We found that prospective wing bud tissue is a high-point of retinoic acid synthesis. Furthermore, retinoid receptor-specific antagonists blocked limb morphogenesis and down-regulated a polarizing signal, sonic hedgehog. Limb agenesis was reversed when antagonist-exposed wing buds were treated with retinoic acid. Our results demonstrate a role of retinoic acid in the establishment of the endogenous zone of polarizing activity.


Development ◽  
1979 ◽  
Vol 50 (1) ◽  
pp. 75-97
Author(s):  
Robert A. Kosher ◽  
Mary P. Savage ◽  
Sai-Chung Chan

It has been suggested that one of the major functions of the apical ectodermal ridge (AER) of the embryonic chick limb-bud is to maintain mesenchymal cells directly subjacent to it (i.e. cells extending 00·4–00·5 mm from the AER) in a labile, undifferentiated condition. We have attempted to directly test this hypothesis by subjecting the undifferentiated subridgemesoderm of stage-25 embryonic chick wing-buds to organ culture in the presence and absence of the AER and the ectoderm that normally surrounds the mesoderm dorsally and ventrally. During the period of culture, control explants comprised of the subridge mesoderm capped by the AER and surrounded by the dorsal/ventral ectoderm undergo progressivemorphogenesis characterized by polarized proximal to distal outgrowth and changes in the contour of the developing explant, and ultimately form a structure grossly resembling a normal distal wing-bud tip. In contrast, explants from which the AER and dorsal/ventral ectoderm have been removed (minus ectoderm explants) or from which just the AER has been removed (minus AER explants) form compact, rounded masses exhibiting no signs of morphogenesis. During the polarized proximal to distal outgrowth control explants undergo during the first 3 days of culture, as cells of the explant become located greater than 0·4– 0·5 mm from the AER, they concomitantly undergo a sequence of changes indicative of their differentiation into cartilage. However, those cells which remain 0·4–0·5 mm from the AER during this period retain the characteristics of non-specialized mesenchymal cells. In marked contrast to control explants, virtually all of the cells of minus ectoderm explants initiate chondrogenic differentiation during the first day of culture. Cells comprising the central core of minus AER explants also initiate chondrogenic differentiation during the first day of culture, but in contrast to minus ectoderm explants, non-chondrogenic tissue types form along the periphery of the explants subjacent to the dorsal/ventral ectoderm. These results indicate that the AER maintains cells directly subjacent to it in a labile, undifferentiated condition, and that when mesenchymal cells are freed from the AER's influence either artificially or as a result of normal polarized outgrowth, they are freed to commence cytodifferentiation. The results further suggest that the dorsal/ventral ectoderm may have an influence on the differentiation of the mesenchymal cells directly subjacent to it, once the cells have been removed from the influence of the AER.


Development ◽  
1981 ◽  
Vol 65 (Supplement) ◽  
pp. 309-325
Author(s):  
Donene A. Rowe ◽  
John F. Fallon

Recent experiments, in which barriers were inserted between anterior and posterior tissues of the chick wing bud, resulted in deletion of structures anterior to the barrier (Summerbell, 1979). From these data it was concluded that blockage of morphogen from the polarizing zone by the barrier resulted in the observed failure of specification of anterior structures. We suggest an alternative interpretation, viz. the interruption of the apical ridge by the barrier caused the deletions. This hypothesis was tested by removal of increasing lengths of ridge. This was done beginning at either the anterior or posterior junction of the wing bud with the body wall and proceeding posteriorly or anteriorly, respectively, to each half-somite level between 16/17 and 19/20. With removal of progressively greater lengths of anterior ridge, more anterior limb elements failed to develop. These data were used to construct a map of the ridge responsible for each digit. To test our hypothesis we removed posterior sections of apical ridge, as described above. Removal of posterior ridge to a level which was expected to allow outgrowth of digits anterior to the level of removal resulted in wings without digits in the majority of cases. An exception occurred when ridge posterior to the mid-19 somite level was removed. In almost half of these cases digits 2 and 3 did develop. In most cases the retention of only a half-somite piece of ridge with all other ridge removed, also resulted in deletion of all digits. Again the exception occurred when ridge posterior to somite level mid-19 and anterior to level 18/19 was removed, leaving only that ridge between somite level 18/19 and mid-19. In many of these cases digit 3 did develop. We conclude from these data that, in the wing bud, ridge anterior to the mid-19 somite level must be connected to more posterior ridge to function. The leg ridge does not exhibit the asymmetrical, low anterior, high posterior configuration, which appears in the wing. Because the leg ridge is symmetrically high anteriorly and posteriorly, we questioned whether or not leg would also require a continuity between anterior and posterior ridge for anterior ridge to function. It did not. When posterior ridge was removed, structures developed under remaining anterior ridge and the elements which developed were complementary to those which developed after anterior ridge removal to the same somite level. Those leg elements, which failed to develop, were truncated at the appropriate proximodistal levels as indicated by the fate map we have constructed for the leg. The data reported here do not rule out a role for the polarizing zone in specification of anterior structures. It is apparent that posterior ridge removal in the wing results in loss of structures anterior to the removal. However, this is not true for the leg.


Development ◽  
1984 ◽  
Vol 80 (1) ◽  
pp. 21-41
Author(s):  
John F. Fallon ◽  
William L. Todt

Histological examination of the stage-18 to stage-23 chick wing bud apex revealed the following. Initially, the wing bud was covered by a cuboidal to columnar epithelium with an overlying periderm. Thickening of the apical ectoderm was not obvious until late stage 18 (36 pairs of somites), after the appearance of the wing bud. At late stage 18, cells of the inner layer of ectoderm had elongated slightly along an axis perpendicular to the epithelial-mesenchymal interface. Well-defined apical ectodermal ridge morphology, i.e., pseudostratified columnar epithelium with an overlying periderm, was not apparent until stage 20. Subsequently the ridge lengthened along the anteroposterior perimeter of the wingbud. We demonstrated histologically that the apical ectodermal ridge of the wing bud was asymmetric with respect to the anteroposterior axis, in that there was more ridge associated with posterior mesoderm. Other observations include the spatial and temporal location of a groove in the base of the thickest part of the ridge. The groove can be correlated with the specification of distal wing elements. The groove was first seen at stage 20 and became more prominent through stage 23. An anteroposterior progression of ectodermal cell death was also observed. This began at late stage 18 and continued through each of the stages examined.


1984 ◽  
Vol 104 (1) ◽  
pp. 111-116 ◽  
Author(s):  
Eugenie L. Boutin ◽  
John F. Fallon

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