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Dependence of the timing system regulating the onset of gastrulation on cytoplasmic, but not nuclear, activities in the Xenopus embryo
Author(s) -
Takagi Makoto,
Shimoda Taiki,
Shinagawa Atsunori
Publication year - 2005
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/j.1440-169x.2005.00808.x
Subject(s) - gastrulation , aphidicolin , embryo , blastula , xenopus , biology , microbiology and biotechnology , cleavage (geology) , vinblastine , andrology , embryogenesis , genetics , cell , medicine , cell cycle , paleontology , chemotherapy , fracture (geology) , gene
This study examines the properties of the timer that regulates the onset of gastrulation in the Xenopus embryo. Pre‐gastrulation embryos were exposed to aphidicolin, vinblastine, 6‐dimethylaminopurine (6‐DMAP) or urethane. Embryos exposed to aphidicolin or vinblastine for 0.5–2 h before the presumptive onset of gastrulation, began gastrulation at the same time as control embryos. However, those exposed to 6‐DMAP or urethane commenced gastrulation significantly later than controls. In 6‐DMAP‐ and urethane‐treated embryos, the onset of gastrulation was retarded by approximately 25% and 120%, respectively. 6‐DMAP and urethane, but not vinblastine, also lowered the rate of nuclear doubling by 30% and 120%, respectively, in late‐blastula to early‐gastrula embryos. 6‐DMAP and urethane also lowered the rate of cleavage and cleavage‐relevant cytoplasmic cycling by 30% and 80%, respectively, in cleavage‐stage embryos. We propose that cytoplasmic activities that can be retarded by 6‐DMAP and urethane, but not aphidicolin or vinblastine, may be responsible for regulating the onset of gastrulation in Xenopus embryos.