TY - JOUR
T1 - Wave propagation in the early stages of aggregation of cellular slime molds
AU - Cohen, Morrel H.
AU - Robertson, Anthony
N1 - Funding Information:
Anyone using cellular slime molds as prototypic organisms for the study of development owes a huge debt to Professors Kenneth Raper and John Bonner. We have benefited both from their published work and their generous donations of time and materials. Dr Brian Shaffer has anticipated many of our quantitative conclusions with his speculations about the nature of aggregative mechanisms; his work is a fertile source of suggestions. We are grateful to Professor Lewis Wolpert for his hospitality, encouragement and stimulating discussion, and we thank David Drage, Dr Brian Goodwin and V. Nanjundiah for help and advice. This research was supported in part by the Office of Naval Research and the Alfred P. Sloan Foundation.
Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1971/4
Y1 - 1971/4
N2 - A detailed theory of the velocity of propagation of the acrasin pulse responsible for the aggregation of some of the cellular slime molds is presented. The ingredients are diffusion of acrasin, triggering after a threshold concentration is reached, an intracellular delay between the reaching of threshold and subsequent release of acrasin, the destruction of acrasin by acrasinase, and an intracellular refractory period. It is suggested that the rate limiting factor in the velocity of propagation is probably the intracellular delay and not intercellular diffusion. It is shown that there is a critical density of amebae below which the waves cannot propagate. The number of neighboring amebae triggered simultaneously by the propagating wave, and therefore the spatial width of the pulse tends to increase with density. Rough estimates are given for the number of acrasin molecules per pulse and for its threshold concentration.
AB - A detailed theory of the velocity of propagation of the acrasin pulse responsible for the aggregation of some of the cellular slime molds is presented. The ingredients are diffusion of acrasin, triggering after a threshold concentration is reached, an intracellular delay between the reaching of threshold and subsequent release of acrasin, the destruction of acrasin by acrasinase, and an intracellular refractory period. It is suggested that the rate limiting factor in the velocity of propagation is probably the intracellular delay and not intercellular diffusion. It is shown that there is a critical density of amebae below which the waves cannot propagate. The number of neighboring amebae triggered simultaneously by the propagating wave, and therefore the spatial width of the pulse tends to increase with density. Rough estimates are given for the number of acrasin molecules per pulse and for its threshold concentration.
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U2 - 10.1016/0022-5193(71)90124-X
DO - 10.1016/0022-5193(71)90124-X
M3 - Article
C2 - 4325172
AN - SCOPUS:0015042105
SN - 0022-5193
VL - 31
SP - 101
EP - 118
JO - Journal of Theoretical Biology
JF - Journal of Theoretical Biology
IS - 1
ER -