Cellular death in morphogenesis of the avian wing

Saunders, John W.; Gasseling, Mary T.; Saunders, Lilyan C.

doi:10.1016/0012-1606(62)90008-8

Cited by 270 publications

(118 citation statements)

References 35 publications

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“…(Saunders et al, 1962;Fallon and Saunders, 1968;Brewton and MacCabe, 1988). In agreement with these studies, we have found that the interdigital tissues are developmentally labile and that they lose their histogenetic potentials gradually and concomitantly with the appearance of cell death in the IDZ.…”

Section: Commitment To Programmed Cell Deathsupporting

confidence: 89%

“…The process frees the digits from each other and helps to form the contours of the mature hand and foot. This self-destruct event does not happen haphazardly in the autopod but occurs at a predicable time and in specific locations as though it has been genetically programmed (Saunders et al, 1962;Saunders and Fallon, 1967;Fallon and Saunders, 1968;Hinchliffe and Thorogood, 1974;Milaire and Rooze, 1983;Milaire, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Influence of digits, ectoderm, and retinoic acid on chondrogenesis by mouse interdigital mesoderm in culture

Lee

Yung

et al. 1994

Developmental Dynamics

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We have cultured tissues isolated from the interdigital zones (IDZ) of the mouse footplate in the presence of the digits, ectoderm, and all-trans retinoic acid. The objective was to understand how these various factors influence the developmental fate of the interdigital tissues. Neutral red staining showed that these tissues normally differentiate by dying between day 12.514.5. However, if they were isolated from the footplate between day 12.5-13.5 (when cell death is not overtly obvious in the IDZ) and maintained in organ culture, these tissues would develop into cartilage and soft connective tissues. In culture, chondrogenesis is initiated very rapidly in the interdigital explants as revealed by in situ hybridization with riboprobes specific for type IIA and IIB procollagen mRNAs. The ability of interdigital tissues to form cartilage is not attributed to factors present in the serum of the culture medium as this phenomenon is also observed in serumless cultures. We have found that if all-trans retinoic acid, at concentrations of 10-50 ng/ml culture medium, were added to the explants it could inhibit chondrogenesis and promote cell death. Moreover, in some of the cultures, a single digit was left attached to the interdigital tissue. This also dramatically reduced the incidence of chondrogenesis. We have tried to determine whether the digits and ectoderm can produce a diffusible factor that can prevent cartilage from developing by culturing day 12.5 interdigital tissues in ectoderm and digit conditioned media. The ectoderm conditioned medium had no effects on interdigital growth or chondrogenesis. In contrast, the size of interdigital explants cultured in the presence of digit conditioned medium was shown to be significantly smaller than the control. These explants also produced a smaller quantity of cartilage as revealed by Alcian blue binding assay. In sum, our results showed that the fate of the interdigital tissues are not fully determined until after day 13.5. These tissues have the potentials to form cartilage and soft connective tissues. We tentatively propose that these interdigital tissues do not normally realize their histogenetic potentials because of the antichondrogenic influence of the digits and retinoic acid.

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Section: Commitment To Programmed Cell Deathsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Influence of digits, ectoderm, and retinoic acid on chondrogenesis by mouse interdigital mesoderm in culture

Lee

Yung

et al. 1994

Developmental Dynamics

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“…In the chick it first appears in the so-called anterior necrotic zone (ANZ), later in the posterior necrotic zone (PNZ), and in the opaque patch (Hinchliffe and Ede, 1973). In the autopod, massive interdigital tissue cell death has been observed (Saunders et al, 1962), and in the mouse this interdigital cell death shows the typical apoptotic nuclei morphology, DNA ladder by electrophoresis, and cytochemical end-labeling of fragmented DNA, which argues that this PCD is apoptotic (Garcia-Martinez et al, 1993;Zakeri et al, 1993;Zakeri et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

“…Early work from Saunders' group (Saunders et al, 1962), indicated that the PNZ was dispensable for chick limb shaping, since if this tissue is removed before cell death takes place, or if the cell death in this tissue is prevented by insertion of a small piece of central meso-derm, a normal wing is formed. Interdigital cell death has long been proposed to be essential for tissue modeling and for digit separation in amniotes (Gilbert, 1997;van der Hoeven et al, 1994), since massive cell death accompanies the formation of free digits in reptiles , birds (Hinchliffe and Ede, 1973), and mammals (Ballard and Holt, 1968;Zakeri et al, 1994), and interdigital PCD is less abundant in animal species with webbed legs (i.e., duck) (Hurle and Colvee, 1982;Pautou, 1973).…”

Section: Introductionmentioning

confidence: 99%

“…Interdigital cell death has long been proposed to be essential for tissue modeling and for digit separation in amniotes (Gilbert, 1997;van der Hoeven et al, 1994), since massive cell death accompanies the formation of free digits in reptiles , birds (Hinchliffe and Ede, 1973), and mammals (Ballard and Holt, 1968;Zakeri et al, 1994), and interdigital PCD is less abundant in animal species with webbed legs (i.e., duck) (Hurle and Colvee, 1982;Pautou, 1973). For example, in the developing chick limb, it has been previously proposed that interdigit degeneration is coincident with digit elongation, resulting in the individualization of digits (Saunders et al, 1962). Furthermore, blockade of BMP signaling has resulted in webbed limbs by apparently preventing cell death (Yokouchi et al, 1996;Zou and Niswander, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Differential tissue growth and patterns of cell death in mouse limb autopod morphogenesis

Salas‐Vidal

Valencia

Covarrubias

2001

Developmental Dynamics

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Programmed cell death (PCD) is considered one of the most important cellular processes in the morphogenesis of organs and tissues during animal development. Although the embryonic limb has been established as a classic model for the study of PCD, detailed studies on this process' contribution to morphogenesis are still lacking. In the present work, using modern computer-aided techniques, we estimated the contribution of PCD to mouse limb morphogenesis. For the detection of apoptotic cell death, we stained whole embryonic limbs with acridine orange or, in some instances, used the TUNEL technique, and visualized the tissues by confocal laser scanning microscopy. We found that cell death patterns are dynamic during limb development, and occur in gradients oriented with the main limb axes, anteroposterior, dorsoventral and distoproximal. Interdigital apoptosis in the autopod was initially detected at the most distal region, and then more proximally as development proceeded. Interestingly, we found that digit separation is more pronounced on the dorsal side, contrary to what is expected from the apoptotic cell distribution, which shows more abundant cell death in the ventral region. Using 2-D and 3-D models, we found that most digit individualization occurs rather by digit growth than by interdigital cell death. Therefore, digits do not mainly individualize by degeneration of preformed interdigital tissue, but probably by a dynamic balance between proliferation and cell death, reducing interdigital growth, which results in protrusion of digits. We determined the expression pattern of fgf-8 during the period of digit individualization, as the product of this gene could participate in defining the limb growth pattern. Initially, fgf-8 expression was coincident with the apical ectodermal ridge, but when cell death was first detected in the interdigits, fgf-8 expression became restricted to the tip of the growing digits. Therefore, FGF-8 could be one of the factors responsible for differential digit-interdigit growth, and might also act as a survival factor on interdigital tissue. We also found that the expression patterns of rar-␤, bmp-2, bmp-4, bmp-7, msx-1, and msx-2 genes, proposed to be involved in the activation of interdigital cell death, did not overlap with, or were not highly expressed in the major zones of cell death in the developing limb.

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Differential expression of TrkC catalytic and noncatalytic isoforms suggests that they act independently or in association

et al. 1998

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Members of the trk gene family encode neurotrophin receptors. The trkC locus encodes multiple neurotrophin-3 catalytic and noncatalytic receptor isoforms. We report the molecular cloning and characterization of mouse cDNAs encoding two noncatalytic TrkC receptors: novel isoforms designated as TrkC NC1 and TrkC NC2, the mouse homologue of the TrkC truncated form previously identified in rat (Tsoulfas et al. [1993] Neuron 10:975-990; Valenzuela et al. [1993] Neuron 10:963-974). We extensively analyzed the transcription pattern of these two noncatalytic isoforms and that of the catalytic isoforms by Northern blotting and in situ hybridization. We did not detect trkC NC1 transcripts in embryos, but we found that trkC NC1 expression is restricted to specific areas in adult brain. In contrast, trkC NC2 transcripts are readily detected early during embryogenesis and are expressed predominantly in adult brain and gonads. We also provide the first evidence for the existence of TrkC NC2 protein by using polyclonal antibodies that specifically recognize this isoform. By using in situ hybridization, we show for the first time that trkC NC2 transcripts are found in differentiating fields of maturing neurons and in mature neurons of laminar structures of adult brain. We also report a similarity of localization between trkC NC2 transcripts and markers of oligodendrocyte progenitors in the embryonic spinal cord. Furthermore, our results also show that trkC NC2 and trkC catalytic transcripts could be either codistributed (in the central and peripheral nervous system) or independently expressed, especially outside the nervous system. These results suggest that the TrkC NC2 isoform acts either independently or in association with its catalytic counterpart. Finally, we show that TrkC NC2 is expressed in dendrites of pyramidal neurons of hippocampus and cerebral cortex. We propose that this receptor is involved in proliferation of oligodendrocyte progenitors, neuronal differentiation, and synaptic plasticity and that it may also play a fundamental role in mediating neurotrophin-3 effects outside the nervous system.

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Cellular death in morphogenesis of the avian wing

Cited by 270 publications

References 35 publications

Influence of digits, ectoderm, and retinoic acid on chondrogenesis by mouse interdigital mesoderm in culture

Influence of digits, ectoderm, and retinoic acid on chondrogenesis by mouse interdigital mesoderm in culture

Differential tissue growth and patterns of cell death in mouse limb autopod morphogenesis

Differential expression of TrkC catalytic and noncatalytic isoforms suggests that they act independently or in association

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