Abstract
During the gastrulation stage in animal embryogenesis, the cells leading the axial mesoderm migrate toward the anterior side of the embryo, vigorously extending cell protrusions such as lamellipodia. It is thought that the leading cells sense gradients of chemoattractants emanating from the ectodermal cells and translate them to initiate and maintain the cell movements necessary for gastrulation. However, it is unclear how the extracellular information is converted to the intracellular chemical reactions that lead to motion. Here we demonstrated that intracellular Ca2+ levels in the protrusion-forming leading cells are markedly higher than those of the following cells and the axial mesoderm cells. We also showed that inhibiting the intracellular Ca2+ significantly retarded the gastrulation cell movements, while increasing the intracellular Ca2+ with an ionophore enhanced the migration. We further found that the ionophore treatment increased the active form of the small GTPase Rac1 in these cells. Our results suggest that transient intracellular Ca2+ signals play an essential role in the active cell migration during gastrulation.
Highlights
Gastrulation is one of the most important processes in the early development of a variety of animals
As chemoattractants for the directed tissue migration, PDGF7 and SDF-111 secreted from the ectoderm have been implicated, and the leading edge mesoderm (LEM) cells are thought to receive these chemokine signals via their respective receptors[8,12]
We found that yellow cameleon (YC)-Nano3GS30 had the most suitable dynamic range, enabling us to detect basal as well as transient increases in the intracellular Ca2+ of LEM tissue
Summary
Gastrulation is one of the most important processes in the early development of a variety of animals. The LEM shows directional migration toward the anterior end on the fibronectin-rich BCR2–5 During this process, axial mesoderm following the LEM undergoes convergent extension, in which cell movements elongate the embryo proper along the anterior-posterior axis and narrow the tissue mediolaterally, eventually forming the rod-shaped notochord[6]. The LEM has an indispensable role in the directional migration of the mesodermal sheet, and disrupting this migration causes severe morphological defects in the embryo, such as abnormal notochord formation and spina bifida[9,10] This anterior tissue migration is thought to be regulated by chemoattractants and/or by cell responses to mechanical signals. We found that Ca2+ transients are required for the polarized lamellipodia formation that accelerates LEM migration Taken together, these results suggest that local Ca2+ signals in LEM cells contribute to the gastrulation cell movements of vertebrates
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