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Journal of Cell Science, Vol 5, 195-210, Copyright © 1969 by Company of Biologists
Submitted on October 14, 1968
1 Biological Laboratories, Harvard University, Cambridge, Massachusetts, U.S.A. and Marine Biological Laboratory, Woods Hole, Massachusetts, U.S.A.; Department of Biology, University of Pennysylvania, Philadelphia, Pennsylvania, 19104, U.S.A.
2 Biological Laboratories, Harvard University, Cambridge, Massachusetts, U.S.A. and Marine Biological Laboratory, Woods Hole, Massachusetts, U.S.A.; Department of Pathology, University of Sydney, Sydney, Australia
In an attempt to understand the mechanism of contraction of the filopodia of the secondary mesenchyme cells and thus secondary invagination of the archenteron, the fine structure of these processes was examined. Whereas microtubules are commonly encountered in the cell body and at the base of the filopodia, very few (one or two) are present near the tip of the filopodia. Instead the slender processes are filled with 50-Å filaments. Colchicine and hydrostatic pressure were applied to the embryos to elucidate the action of these different fibrous elements. Both agents cause cessation of archenteron movement and the disassembly of the microtubules. Hydrostatic pressure causes the disappearance of the filaments as well. Because of the small numbers of microtubules in the slender filopodia and the fact that in no other system is there any evidence for contraction of these elements, it was concluded that they do not function in the contraction process, but are probably involved in the formation of these cell extensions: hence the effect of colchicine on archenteron movement. The 50-Å filaments, on the other hand, are likely candidates for the contraction process.
Submitted on October 14, 1968