Mitosis and cell death in the tail of the chick embryo

Abstract

Although somites develop from the mesoderm in the tail of the chick embryo, they do not form to the tip of the tail. Previous work has shown that this terminal mesoderm possesses many of the characteristics of the segmental plate mesoderm which gives rise to the somites in the trunk. This investigation is aimed therefore at understanding why the terminal mesoderm fails to form somites. Mitotic and pyknotic rates have been obtained for the tail region of chick embryos between stages 13 and 27. Embryos were treated with colchicine, so that the mitoses were blocked in metaphase, and counts were made on serial sections. The overall mitotic rates were highest between stages 15 and 18. Regions of high mitotic rate, which are an indication of cell synchrony, were found in the tail bud mesoderm though not in a consistent location, and only infrequently near the anterior end of the tail segmental plate. In the trunk however (Stern and Bellairs 1984) a single peak of cell synchrony was routinely found near the cranial end of the segmental plate. It is concluded that the cells of the tail mesoderm are less synchronised in preparation for somitogenesis than are the corresponding mesoderm cells in the trunk. A further conclusion is that the tail bud is not per se a region of high proliferation, though there are patches of high mitotic rate. The overall pyknotic rate reached a maximum at stage 25; peaks of pyknosis corresponded initially with the mitotic peaks and were associated with the ventral ectodermal ridge and the tail gut. By stage 25 however, the high levels of cell death were restricted mainly to the tip of the tail.(ABSTRACT TRUNCATED AT 250 WORDS)

Stem cells, signals and vertebrate body axis extension

“…This might elicit a slowing down of the cell cycle and the eventual cell cycle exit of progenitor cell populations. Conversely, the loss of Fgf8 also coincides with high levels of cell death in the late-stage chick tail bud (Hirata and Hall, 2000;Mills and Bellairs, 1989;Sanders et al, 1986;Yang et al, 2006), raising the possibility that a local increase in endogenous RA triggers apoptosis to terminate axis extension.…”

Cessation of gastrulation is mediated by suppression of epithelial-mesenchymal transition at the ventral ectodermal ridge

“…Accompanying the elongation of the tailbud, the remnant of the primitive streak is progressively involuted toward the ventral region of the tailbud, resulting in the formation of the chick VER in the ventral tail region during HH stage 16-18 (the blue region at HH stage 16 and 18 in Fig. 1A) (Catala et al, 1995;Mills and Bellairs, 1989). It is thought that the chick VER finally disappears through cell death by the stage when most of the somites have formed (HH stage 24, Fig.…”

Spatiotemporal distribution of apoptosis during normal cloacal development in mice

“…In addition, for the formation of various structures during morphogenesis, cell death occurs according to precise temporal sequences and spatial patterns and is considered to play a key role by elim- inating unnecessary cells to achieve complex histogenesis and organogenesis. For example, cell death is involved in remodeling the embryonic tail bud in humans (Kunimoto, 1918;Wittman et al, 1972;Fallon and Simandl, 1978), mice (Wittman et al, 1972;Schoenwolf, 1984;Tam, 1984), rats (Butcher, 1929;Gajović et al, 1989Gajović et al, , 1993Qi et al, 2000b), and chicks (Klika and Jelinik, 1969;Van Horn, 1971;Schoenwolf, 1981;Sanders et al, 1986;Mills and Bellairs, 1989;Miller and Briglin, 1996). Several investigators have indicated that cell death is involved in removal of the tailgut in chicks (Van Horn, 1971), rats (Š vajger et al, 1985), and humans (Fallon and Simandl, 1978).…”