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THE CONTRACTILE PROCESS IN THE CILIATE, STENTOR COERULEUS : I. The Role of Microtubules and Filaments

The structural basis for the function of microtubules and filaments in cell body contractility in the ciliate Stentor coeruleus was investigated. Cells in the extended state were obtained for ultrastructural analysis by treatment before fixation with a solution containing 10 mM EGTA, 50–80 mM Tris,...

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Detalles Bibliográficos
Autores principales: Huang, B., Pitelka, D. R.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1973
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2108994/
https://www.ncbi.nlm.nih.gov/pubmed/4633444
Descripción
Sumario:The structural basis for the function of microtubules and filaments in cell body contractility in the ciliate Stentor coeruleus was investigated. Cells in the extended state were obtained for ultrastructural analysis by treatment before fixation with a solution containing 10 mM EGTA, 50–80 mM Tris, 3 mM MgSO(4), 7.5 mM NH(4)Cl, 10 mM phosphate buffer (pH 7.1). The response of Stentor to changes in the divalent cation concentrations in this solution suggests that Ca(+2) and Mg(+2) are physiologically important in the regulation of ciliate contractility. The generation of motive force for changes in cell length in Stentor resides in two distinct longitudinal cortical fiber systems, the km fibers and myonemes. Cyclic changes in cell length are associated with (a) the relative sliding of parallel, overlapping microtubule ribbons in the km fibers, and (b) a distinct alteration in the structure of the contractile filaments constituting the myonemes. The microtubule and filament systems are distinguished functionally as antagonistic contractile elements. The development of motive force for cell extension is accomplished by active microtubule-to-microtubule sliding generated by specific intertubule bridges. Evidence is presented which suggests that active shortening of contractile filaments, reflected in a reversible structural transformation of dense 4-nm filaments to tubular 10–12-nm filaments, provides the basis for rapid cell contraction.