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  • Life and Medical Sciences  (2)
  • Ca2+-dependent K+ channels  (1)
  • 1
    ISSN: 1432-1424
    Keywords: calmodulin ; Ca2+-dependent K+ channels ; ion channel regulation ; mutations ; Paramecium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Paramecium tetraurelia possesses two Ca2+-dependent K+ currents, activated upon depolarizationI K(Ca,d), or upon hyperpolarizationI K(Ca,h). The two currents are mediated by pharmacologically distinct ion channel populations. Three mutations ofP. tetraurelia affect these current.s Pantophobiac A mutations (pntA) cause calmodulin sequence defects, resulting in the loss of both Ca2+-dependent K+ currents. A second mutation, TEA-insensitive A (teaA), greatly enhancesI K(Ca,d) but has no affect onI K(Ca,h). A third mutation,restless (rst), also increasesI K(Ca,d) slightly, but its principle effect is in causing an early activation ofI K(Ca,h). Interactions between the products of these three genes were investigated by constructing three double mutants. BothteaA andrst restoreI K(Ca,d) andI K(Ca,h) in pantophobiac A1, but the phenotypes ofteaA andrst are not corrected by a second mutation. These observations may indicate a role for the gene products ofteaA andrst in regulating the activity ofI K(Ca,d) andI K(Ca,h), respectively.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 2 (1982), S. 217-224 
    ISSN: 0886-1544
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 4 (1984), S. 283-295 
    ISSN: 0886-1544
    Keywords: axonemal mutants ; Ca++ response ; ciliary reversal ; electrophysiology ; models ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Six mutants of Paramecium tetraurelia, which display altered axonemal responses to Ca++, are described. The mutants, designated atalantas, are impaired in their ability to swim backward when stimulated by ions or heat; instead they spin very rapidly in one place. Three mutants, ataA1-3, are completely unable to swim backward. The three lines, however, can be distinguished from one another by their forward swimming velocities. The remaining three mutants are leaky. ataB swims backward briefly when stimulated, then stops and spins in place. ataC and ataD are extremely leaky and only display the spinning phenotype at elevated temperatures. An electrophysiological analysis reveals that all six mutants have normal membrane properties, including the Ca++ inward current under voltage clamp. When the membrane is disrupted so as to allow the axoneme free access to Ca++, wild-type cells swim backward, but the mutants do not. These data indicate the site(s) of lesion in the mutants is in the axoneme or in some step linking Ca++ influx and the axoneme, not within the ciliary membrane. These mutants may be useful in investigating the role of Ca++ in the regulation of axonemal motion.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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