A cell cycle arrest is necessary for bottle cell formation in the early Xenopus gastrula: integrating cell shape change, local mitotic control and mesodermal patterning.
During development cell proliferation and morphogenetic movements are tightly intermingled. Both processes depend on the same cytoskeletal elements. Therefore, precise regulation of local mitotic activity seems to be basic for proper embryogenesis. Here, I report on bottle cells as an early non-mitotic cell population in the Xenopus gastrula. Endogenous and activin/BVg1-induced ectopic bottle cells do not proliferate. Overexpression of the mitosis-promoting phosphatase cdc25C increases the proliferation rate and interferes with bottle cell formation whereas the phosphatase-dead mutant cdc25C(C457A) does not. Cdc25C also affects other gastrulation processes such as epiboly, vegetal rotation or tissue separation as inferred from histological inspection of early gastrulae. Double stainings of gsc/Xbra transcripts and mitotic nuclei in ectopic and endogenous lips demonstrated that non-mitotic cells occur in the bottle cell region and, to a lesser extent, in the gsc domain which both are indicative of high TGF-beta signalling. In contrast, the Xbra-region and the remainder of the animal cap appear to be permissive for higher rates of cell proliferation. These data suggest inhibition of cell proliferation by high levels of activin-type signals and a close link of mesodermal and mitotic patterning. Finally, coexpression of eFGF together with activin/BVg1 interferes with TGF-beta-induced bottle cell formation. This inhibitory effect correlates with increased cell proliferation as compared to embryos injected with activin/BVg1 alone. Taken together, these data suggest that TGF-beta and FGF signals play antagonistic roles in bottle cell formation and the spatial control of the cell cycle in early Xenopus gastrulae.[1]References
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