A proposed role for the Ca ion in the chemotactic response of Physarum polycephalum

Bibliography: pages 107-111. === Durham, in a review published in 1974, presented the following hypotheses concerning the factors that control amoeboid movement: (1) actin and myosin are present in all cells that exhibit amoeboid movement and, changes in the internal [Ca⁺⁺] regulate contraction, (2)...

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Bibliographic Details
Main Author: Ludlow, Christopher Trimble
Other Authors: Van Regenmortel, M H V
Format: Dissertation
Language:English
Published: University of Cape Town 2016
Subjects:
Online Access:http://hdl.handle.net/11427/22333
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Summary:Bibliography: pages 107-111. === Durham, in a review published in 1974, presented the following hypotheses concerning the factors that control amoeboid movement: (1) actin and myosin are present in all cells that exhibit amoeboid movement and, changes in the internal [Ca⁺⁺] regulate contraction, (2) filaments of actin and myosin form an intimate association with the surface membrane and depending on the local [Ca⁺⁺] , the filaments can cause the membrane to relax or become rigid, (3) Ca⁺⁺ fluxes across the external membrane (viz. efflux and influx) regulate the state of contraction in the proposed actinomyosin-surface membrane network and, (4) such Ca++ fluxes operating across the membrane manifest themselves (especially with slime mould plasmodia) as waves of adhesion running across the undersurface of a cell and aid in movement. A working hypothesis, that encompasses the ideas of Durham, is that Ca⁺⁺ entry and efflux across the external membrane control such cellular processes as extension of pseudopodia, exocytosis, endocytosis and the direction of movement (chemotactic response) of amoeboid cells. In the specific case of slime mould plasmodia, which best exemplify all of Durham's hypotheses, the simplest hypothesis to explain the control of chemotaxis is that attractants (sugars, food; organisms) cause a Ca⁺⁺ efflux across the membrane and a subsequent movement forward. Repellents would act in a reverse manner by causing Ca⁺⁺ entry. This hypothesis also allows for the existence of a Ca⁺⁺-accumulating organelle. This organelle might replace or act in concert with the proposed Ca⁺⁺ fluxes across the external membrane. The investigations reported in this thesis were devised to examine experimentally this hypothesis.