Removal of transient features in morphogenesis of chick embryo tail is by programmed cell death. We used ApopTag™ (Oncor®, Gaithersburg, MD) with the peroxidase/diaminobenzidine (DAB) procedure to correlate apoptosis with earlier reports of patterns of cell death in stage HH17–25 embryos, and our results suggest that the cell death inferred with supravital staining and appearance of cells in morphogenesis of the tail bud is programmed cell death called apoptosis.
Apoptosis markers in tail bud are most abundant in the median cell cord of occluded, degenerating tail gut. Tail bud mesenchyme marks for apoptosis most frequently in the ventrum of older stages, where cell death has been reported. Cells of the remnant of the primitive streak (Hensen's node) mark for apoptosis, suggesting that programmed cell death is a stop signal for axial organization at the caudal terminus. Apoptosis markers in postmembrane cloacal endoderm anticipate the transient cloacal fenestra. Lack of apoptosis markers in neural tube, notochord, and somites supports the suggestion of Schoenwolf ( Anat. Embryol. (Berl.) 162:183–197) that cells of those areas in the tail bud are assimilated into the growing rump of the chick embryo. Lack of markers in neural tube of tail bud formed by secondary neurulation suggests that apoptosis is not involved in cavitation of medullary cord, but further investigation is necessary.
A limited investigation of pharyngeal membranes and midgut, where cell death has not been reported to be as important in morphogenesis, did not show apoptosis markers in those tissues (Miller and Briglin  “Cell Death in Development and Cancer,” Houston: University of Texas MD Anderson Cancer Center, pp. 82–83). Absence of apoptosis markers in roof of gut tube suggests that the lower frequency of thymidine labeling reported for those cells (Miller  Anat. Rec. 214:87A) is not a result of apoptosis. Clearly marked cells correlated with expected locations of migrating neural crest and primordial germ cells in these stages, but distribution of apoptosis markers was not abundant or general for either cell type. © 1996 Wiley-Liss, Inc.